Immunology Flashcards
(88 cards)
1
Q
Hemopoietic Cell Origins
A
Stem Cells: All blood cells arise in the bone marrow from stem cells - undifferentiated bone marrow cells that self-renew
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Q
Hemopoietic Cell Origins
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At division two daughter cells are produced; one daughter cell matures into the various blood cells after passing through a series of steps; the second daughter cell become the new stem cell
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Q
Types of blood cells:
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Leukocytes (white blood cells)
Erythrocytes (red blood cells)
Thrombocytes or platelets (which are fragments of a precursor cell - the megakaryocyte)
4
Q
Myeloid progenitors
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Develop into cells of the Innate Immune system. Monocytes/Macrophages; Neutrophils; Eosinophils; Basophils/Mast cells. Leukemia involving these cell lines are known as acute/chronic myelocytic leukemia
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Q
Lymphoid progenitors
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Develop into lymphocytes, member of the adaptive immune system. Leukemia involving these cells lines are referred to as acute/chronic lymphocytic leukemia
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Q
“Blast”
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A very immature blood cells –when observed in a peripheral blood smear, or increased numbers in a bone marrow aspirate - reflects a leukemic state
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Q
Immune cells are sometime classified by the presences or absences of large granules in their cytoplasm
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Granulocytes: Neutrophils, eosinophils, basophils/mast cells
Agranulocytes: Lymphocytes and Monocytes
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Q
Cytokines
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Diverse and potent chemical messengers produced primarily by the cells of the immune system. Cytokines function as hormone like signals between cells of the immune system. They are the chief communication signals of the T cell. Cytokine binding to specific receptors on target cells results in recruitment of other cells to the battle field, promotion cell activation, encouragement of cell growth, and direction of cellular traffic. There are a great number of known (and likely a greater number of undiscovered) cytokines.
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Q
Commonly known cytokines:
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The Interferon family
The Interleukin family
Tissue necrosis factor (TNF)
Growth factors
- Granulocyte Colony Stimulating Factor (GCSF)
- Granulocyte Macrophage Colony Stimulating Factor (GM-CSF)
10
Q
Lymphokines
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Are cytokines secreted by T and B cells (lymphocytes)
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Monokines
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Are cytokines secreted by Monocytes and macrophages
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Q
Interleukins
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Messenger between leukocytes (WBC’s)
13
Q
Chemokines
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Cytokines that attract specific cells to an area. They are release at the site of infection/injury and call other cells to the area
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Q
Although we emphasize the cytokine role in immune system communication, it is important to keep in mind their roles in influencing local area dynamics (increased capillary permeability, vaso dilatation etc.) and systemic influences, (fever, influencing prostaglandins, etc.)
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Although we emphasize the cytokine role in immune system communication, it is important to keep in mind their roles in influencing local area dynamics (increased capillary permeability, vaso dilatation etc.) and systemic influences, (fever, influencing prostaglandins, etc.)
15
Q
Physical Barriers
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The first line of defense
o Skin covers about 2 square meter
o Mucous membranes covers about 400 square meters
o The structure of skin and mucous membrane are physical impediments to invasion. Additionally these structures secrete substances producing an inhospitable environment for microbes. (ex. low pH, mucous, fatty acids, etc.)
16
Q
Innate Immune System
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The second line of defense; Nonspecific in focus and “Always on” - ready to protect us from invasion. Generally composed of: o Macrophages o Neutrophils o Natural Killer Cells o Eosinophils o Basophils o Mast Cells o The Complement System
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Q
The Adaptive Immune System
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The third level of defense
o Defends against specific invaders – Edward Jenner and his work with the small pox vaccine in 1790 is a classic example of an adaptive immune response
o Composed of Lymphocytes
18
Q
T Cells
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(Thymus derived lymphocytes) subdivided into:
- T helper cells (aka. Th, CD4 cells)
- Cytotoxic Lymphocytes or Killer T cells (CD8 cells)
- Regulatory T cells
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Q
B Cells
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(aka. Bursa or Bone marrow derived lymphocytes)
- When a B cell is activated and producing antibodies it is often referred to as a Plasma cell.
20
Q
Macrophages
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Long lived cells which are very active phagocytes ingesting microorganism and cellular debris.
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Q
Macrophages
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First exiting the bone marrow and circulating in the blood are called Monocytes. They slip between the endothelial lining of capillaries into tissues where they mature into macrophages.
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Q
Dendritic cells
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Is the general name of tissue macrophages. Tissue macrophages often have particular names associated with particular tissues: lung -alveolar macrophages; liver - Kupffer cells; central nervous system – microglia; Macrophages are abundant in the lining of lymph nodes and spleen, epidermis and mucous membranes –esp. anal, vaginal, and oral areas. Some are fixed to the tissues, other are “wandering macrophages”
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Q
Macrophages
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o Actively seek invaders and scavenges for “garbage”
o Sequence: Phagocytosis – “to eat”
Bacterium outside macrophage, Macrophage engulfs bacterium in a phagosome, Phagosome taken inside the macrophage, Phagosome fuses with a lysosomes, Enzymes in lysosomes digest bacterium
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Q
Macrophages
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Once the macrophage phagocytizes a cell, it transports some of the invader’s proteins to its surface to show and stimulate other immune cell. Macrophages are important Antigen Presenting Cells (APC)
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Macrophages
After battling with bacteria, macrophages give off cytokines that are important mediators of the inflammatory response
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Neutrophils
An aggressive phagocyte
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Neutrophils
Aka. Polymorphonuclearcytes (“polys”); polymorphonuclear neutrophils (PMN); segmented neutrophils (mature neutrophils); “bands” (neutrophils without segmentation, a reflection that they are very recently produced).
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Neutrophils
o Short lived (3-5 days). Depends on glycogen stores for energy
o Very active phagocytes
o Comprise 70% of WBC in blood – we normally see 70% polys on a peripheral smear blood count with 1-2% bands forms
o The presences of an increased percentage of “bands” in a blood smear indicates a ramping up of the immune response to bacterial infection and is referred to as a “Shift to the left”
o PMN’s are attracted to cytokines such as TNF, interleukin 1 produced by macrophages and others
o They do not function as antigen presenting cells
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Natural Killer Cells
o Difficult to study ( they are lymphocyte like and difficult to differentiate from B and T cell to study )
o Once NK cells exit the vessels and are in tissue, they are very versatile -they can kill tumor cells, virus-infected cells, bacteria, virus, fungi, and parasites; they kill infected cells by instructing them to commit suicide. (apoptosis)
o Given NK cell’s power /versatility a two signal system is needed for control – a balance between “kill’ and “don’t kill” signals determines whether a NK cell will destroy a target cell
o NK cells recognize and attack cells lacking “self” markers. (If the cell does not have normal “this is me” antigens, NKC will kill the cell without prompting from other immune sources. (This is a different from cytotoxic lymphocytes who have similar functions, but require prompting from other immune system cells)
o Some NK cells function as cytokines factories
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Eosinophils
o Granule containing cells which circulate in low levels in the blood stream. Important in allergic phenomena and particularly important in combating parasites
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Basophils and their cousin, the Mast cells
o Stationed primarily in the tissues. Contain granules loaded with histamine, leukotrienes and other allergy related chemicals. Very important in allergic phenomena.
o If a parasite invades tissue, mast cell attempt to neutralize the invader by dumping their contents onto them
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Pattern-Recognition Receptors
Cells of the innate immune system are able to bind to antigens using inherited pattern-recognition receptors. These receptors are encoded in the germ line of each person and are passed from generation to generation. As our species evolved, receptors for pathogen associated molecular patterns developed via natural selection to be specific to certain characteristics of broad classes of infectious organisms. Receptors to bacterial cell wall lipopolysaccharides and peptidoglycans, bacterial DNA, dsRNA and many other substances are present on our immune cells
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The Complement System
o Composed of approximately twenty different proteins that work together to destroy invaders and signal other immune system components that an attack is on. These are proteins produced primarily by the liver and present in high concentrations in blood and tissues. C3 is the most abundant compliment protein.
o A spontaneous and very fast system
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Activation of complement (the functioning of compliment) may result in:
o Opsonization of the invader
o Chemo-attraction of other killing cells
o Lyses of the cell /virus: Activation of the complement cascade result in the production of a “membrane attack complex” which opens up a hole in the surface of the bacterium/virus killing it.
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Compliment activation may occur by several pathways:
o “Classic” pathway – depends on the presences of antibody-antigen complexes for activation of compliment
o Alternative pathway – C3 will attach to any “unprotected” cells, resulting in a cascade of compliment activation (destroying any unprotected surface). Stated a second way, any cell surface that is not “protected” will be attacked by compliment. Protected cells have certain proteins on their surfaces (ex. DAF –decay acceleration factor; CD59-protectin) that control compliment activation. Human cells are covered with protective substances which keep the positive feedback loop of complement activation from gaining a foothold and taking off.
o Lectin Activation Pathway –Patterns of carbohydrates and fats on the surface of common pathogens (bacteria, fungi) activate mannose binding lectin (MBL -produced in the liver) which in turn actives the complement cascade.
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Cells of the Adaptive Immune system
Response is slow and specific
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T Lymphocytes (“T cells”)
Responsible for “Cell Mediated Immunity”
o T cell response is slow and specific by clonal selection and modular design
o Antigens must be “presented” to the T cell for T cell activation
o Only recognizes protein antigens
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Helper T cells (Th)
o Coordinators of the immune system response
o Identified by CD4 receptors on cell surface.
o Th read the MHC II of “antigen presenting cells” (macrophages) which activates the Th
o Th cells direct action by secreting cytokines that have dramatic effects on other immune system cells.
o Examples of cytokines produced by Th cells: IL-2,4,5,10, IFN, TCF
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Killer T Cell or cytotoxic lymphocytes
o Identified by CD8 receptors on cell surface
o Important in eliminating virus infected cells.
o Activation is a two part process: Read the MCH I of a cell AND Receives input from a Th cell
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Regulatory T cells (aka. Treg; suppressor T cells)
o Poorly understood; difficult to study
o Identification is difficult. Some by CD4, CD 25 Foxp3, CTLA4, Transforming Growth Factor-beta (TGF-β)
o Function in suppression (control) of immune response
o Have a role in tolerance to self-antigens: Some autoimmune diseases may be the result of malfunction with Treg cells
o Research interest in modifying activity of Treg cells as a treatment for cancer
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“B Lymphocytes” (“B cells”)
Responsible for “Humoral Immunity”
o Mature in the bone marrow (Bursa cells)
o Activation results in production of antibodies to foreign organic molecules
o Activated B cells which are producing antibodies often referred to as “Plasma Cells”
o Th input is important in activation
o They are capable, under certain conditions, of recognizing an antigen by itself (does not necessarily need T helper cells (Th) input
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Memory Cells
Once a lymphocyte is “activated” it proliferates rapidly producing a clone of lymphocytes. When no longer needed, the clone generally dies off by apoptosis leaving a few memory cells. Since memory cells have gone through the process of activation, they are able to quickly and efficiently mount response to invader they recognize (the basis for the use of vaccines).
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Antibodies and Immunoglobulins
Antibodies are also referred to as Immunoglobulins (Igs). An immature B cell is stimulated to mature, or to become “activated” when it binds to a foreign organic molecule (antigen; vs. T cells which only bind to foreign proteins) and a Th cell signals it to become activated. This process “sensitize” or “primes” the B cell. The B cell will produce a large “clone” of identical cells, most of which will become “Plasma Cells” which produce large quantities of specific antibodies (each producing 2000 molecule per second). The process to gear up to maximum antibody production is slow (? 5-10 days). Following resolution of the infection, a few of the “clones” will become long lived
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Memory Cells
Are ready to ramp up in a very short time should the host be challenged by the same antigen in the future. The memory cell response can be so quick, one never experiences any symptoms of that particular infection.
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Structure of antibodies:
heavy chains and light chains. The two “hands” of the light chain can bind to antigens (Fab); a receptor region on the tail (Fc)which are heavy chains, binds to the surface of other immune systems cells.
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Function of antibodies:
Antibodies inactivate antigens by:
- Promoting compliment fixation
- Agglutination (clumping)
- Precipitation (forcing insolubility and precipitation out of solution)
- Act as an opsonizer (preparing to eat)
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IgG
The most abundant immunoglobulin in the serum; also able to enter tissues
- The only antibody that crosses the placenta and is responsible for 3-6 months of immune protection in the newborn
- helps NK cells; good opsonizer
- The presences of a particular IgG antibody in serum is generally indicative of past infection (recent past or distant past)
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IgM
- The first antibody produced in an immune response
- Very large molecule and tends to remain in the blood stream
- Presence is indicative of current infection
- Great compliment fixer
- Good opsonizer
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IgA
- Guards the mucosal surfaces of the body including digestive, respiratory, and reproductive
- The most abundant antibody produced (consider the 400 square meter of mucosal surface)
- Can be transported across intestinal wall into the intestinal lumen. The IgA “coats” invading pathogens and prevent attachment to intestinal walls. Ditto respiratory/reproductive tracts
- The most abundant antibody “outside the body”
- They tend to agglutinate the bacteria into clumps that are swept out of the body with the mucus.
- Secreted into the milk of nursing mothers protecting baby from pathogens
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IgE
- 0.002%
- Important in anaphylaxis and allergy
- Allergens may be mistaken for an invader
- With initial exposure to an allergen, some individual produce large quantities of IgE
- Mast cells have surface receptors that will bind with the Fc region of IgE antibodies. On second exposure to the allergen, IgE will bind the allergen resulting in mast cell degranulation of histamine and other chemical that increase capillary permeability. As a local effect we may get a runny nose, watery eyes or a local area of hives. In anaphylaxis there is a massive degranulation of mast cells resulting in bronchospasm, hypotension, and CV collapse.
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IgD
Poorly understood; may act as a receptor when attached to B cells and an activator of other cells.
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Major Histocompatibility Complex proteins (MHC)
MHC are proteins that all cells display on their surfaces which as a total, are effectively unique to that individual. It is the MHC complex which allows our immune system to differentiate “self” from “non self”. Any cell displaying that person’s MCH type belongs to that person (and is therefore not an invader)
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Major Histocompatibility Complex proteins (MHC)
As scientists studied the MHC of leukocytes, they developed a system of antigens known as Human Leukocyte Antigen (HLA) system. In other words, the HLA system is the MHC of leukocytes. (WBC’s are convenient cells to study, and since each normal cell in an individual will have the same antigens, HLA will be the same as the individual’s MHC)
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Class I MHC
Molecules are found in varying amounts on the surfaces of all nucleated cells (RBC’s don’t have nuclei) and function as billboards that inform killer T cells about what is going on inside the cell. If a virus infects a cell, some viral fragments are loaded onto the Class I MHC molecule and transported to the cell surface for display. Infected or otherwise abnormal cells can be recognized and destroyed by components of the immune system. Killer T (CD8) cells can use their receptors to effectively” look into” the cell to determine that it is infected and should be destroyed
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Class II MHC
Molecules also function as billboards, but this display is intended only for the Th (helper T cell) use. Only certain cells make class II MHC and these are known as antigen presenting cells (APC). A macrophage will phagocytize a bacterium and load some bacterial fragments (peptides) onto the MHC II molecules which it displays on its surface. Th cell will scan the macrophages MHC II molecules and direct the immune system to take action against the infection
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Graft rejection
Any cell displaying some other MHC type (HLA type) is “non-self” and is an invader, resulting in varying degrees of rejection of the tissue bearing those cells.
- Tissue typing and matching is an attempt to find the best match of HLA antigens between donor and recipient.
- Most anti-rejection drugs function to dampen the normal immune response to foreign materials to prevent rejection.
- As we purposely impair the immune response to prevent/delay rejection, we need to be mindful that we have also impaired the immune response to all invaders – the immunocompromised patient
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Graft vs. Host disease
May occur in bone marrow transplantation, or blood transfusion in severely immunocompromised patients. Cytotoxic T cell in the ‘graft” (transfusion) attack the recipient’s cells
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Autoimmunity
Autoimmune disorders occur when the immune system no longer recognizes “self” and mounts an attack (in varying degree) to our own tissues. A few examples include: Type I Diabetes, Celiac Disease, SLE (Lupus erythematous), Myasthenia Gravis, Sjogren’s syndrome, Rheumatoid arthritis, post streptococcal glomerulonephritis, sympathetic opthalmia.
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Autoimmunity
- Some inherited HLA types are associated with autoimmune disorders. In a person with the HLA B-27 antigen there is a strong association with ankylosing spondylitis (“Bamboo spine”).
- Treatment/research areas include suppressing the immune response, or attempting to modulate the immune response
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Pathophysiology: auto immune diseases
Molecular mimicry
b. Myasthenia gravis
c. Lupus erythematous
d. Rheumatoid arthritis
e. Transplanted organ rejection
f. Some forms of Type I diabetes mellitus
g. Anti-thyrotropin receptors in some thyroid disease
i. Associated with genetic factors HLA-B8 (MSH classI) HLA-DR3 MCH class II
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Cancer and Immune surveillance
- Cells with abnormal growth patterns (cancer) may display abnormal MHC patterns on their surface. Our immune system recognizes these abnormal cells and targets them for apoptosis - destroying/controlling many cancers before reach a stage where they are clinically diagnosis.
- Certain HLA types are associated with various cancers (ex. T cell lymphoma and HLA DR3-DQ2).
- There continues to be great interest in methods to develop an immune response to tumor antigens. Ex: “Cancer vaccines”
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Activation of the Adaptive Immune System
Collectively B and T cells are known as lymphocytes. They must be activated before they can function
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Activation of the Adaptive Immune System Sequence
1. Activation of helper T cell:
2. Helper T cell recognition of an antigen displayed by class II MHC molecules on the surface of an antigen presenting cell. PLUS: A second signal or “key”. This is non-specific and involves:
A protein on the surface of the of the antigen presenting cell(B7) that plugs into: receptor of the helper T cell (CD28)
3. Once helper T cells are activated by the two key system, it proliferates building a clone of many helper T cells that recognize the same antigen.
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The Inflammatory Response
This is a general term that describes the battle scene between the immune system and infectious agents. There exists a range of responses from mild to very dramatic. Components responsible for an inflammatory response include:
o The cellular response of macrophages, neutrophils, other immune cells to infection which promote release of histamine, bradykinin, serotonin and many other vasoactive substances.
o Cytokine production by various immune cells produce TNC (tissue necrosis factor), IFN (interferon gamma), IL (interleukin)-2,4,5 6…. and others not only influence other immune system cells, but act on tissues on both a local level and systemic level
o Activation of the compliment system
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Rubor, Dolor, Calor
Are the hall mark physical finding of the inflammatory response
o Increased local blood flow – erythema, warmth
o Increased permeability of blood vessel, promoting movement of immune cells into tissue resulting in edema, and pus (mainly spent neutrophils)
o Stimulation of nerves in the tissue: nociceptive stimulation (pain)
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The Inflammatory Response
Clinically we look for sign of the inflammatory response when we suspect infection (what are the common physical finding of furunculosis (boils) or an infected cut?)
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The Inflammatory Response
Autoimmune diseases often have a longer term “indolent” type of inflammation which suggest the classic “inflammatory response”, but may appear much more subtly. The chronic nature of the milder immune response to the synovial lining of joints results in the clinical picture of Rheumatoid arthritis
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The Inflammatory Response
In some circumstances the immune response itself is part of the pathogenesis of disease. A vigorous immune response may result in tissue damage beyond the damage caused by the infectious agent itself. As an example, a patient with a severe pneumonia is sometime treated with steroids (and antibiotics or antivirals) attempting to dampen the immune response to the infection.
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Type I Hypersensitivity Reaction
o Acronyms: “immediate” or “anaphylactic”
o IgE and mast cell/basophil mediated
o Usually occur in 5-30 minutes time frame; can be “delayed” 10-12 hours
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Type I Hypersensitivity Reaction
Signs and symptoms are related to histamine and other agents from degranulation of mast cells:
• Dyspnea, bronchospasm
• Urticaria/angioedema
• Visceral edema
• Hypotension (dilated, leaky blood vessels result in decrease cardiac afterload and decreased cardiac preload)
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Type II Hypersensitivity Reaction (“antibody-dependent”)
o A result of development of antibodies to cell surface antigens
o IgM or IgG mediated
o May affect a variety of organs and tissues
o Time frame: minutes to hours to days
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Type II Hypersensitivity Reaction (“antibody-dependent”)
Examples:
• Transfusion reactions
• Drug induced autoimmune hemolytic anemia
• Autoimmune thrombocytopenia, granulocytopenia,
• Good pasture’s nephritis
• Pemphigus
• Acute rheumatic fever
• Myasthenia gravis
• Graves’ disease (an auto immune thyroid disorder)
o Biopsies of skin lesions contain antibody, complement, and neutrophils/macrophages
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Type III Hypersensitivity Reaction (immune complex)
o Disease caused by production of circulating “immune complexes” of antigens and antibodies
o The antigen-antibody complexes precipitates out of solution and are deposited in tissues. Complement is activated by this “immune complex” which result in inflammation (inflammatory reaction)- neutrophils /macrophage /cytokines and platelet aggregation
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Type III Hypersensitivity Reaction (immune complex)
```
Often involves individual organs including skin, kidneys, lungs, blood vessels and joints. Examples include:
o Systemic lupus erythematosus (SLE)-skin, kidney & others
o Polyarteritis (blood vessel involvement)
o Rheumatoid arthritis (joint involvement) (?)
```
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Type III Hypersensitivity Reaction (immune complex)
Occasionally presents as a generalized reaction known as serum sickness
o Presents with fever, arthralgia, lymphadenopathy, rashes, etc.
o Rabies antitoxin (derived from horse serum) is a classic example of an agent inducing serum sickness
o Many drugs have been implicated
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Type III Hypersensitivity Reaction (immune complex)
Diagnosis (Dx)
o Tissue biopsies with staining for immune complexes reviewed microscopically
o Immune complexes detected in serum
o Depletion of compliment (check serum C3 or C5 levels)
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Type IV Hypersensitivity Reaction
o Acronyms : “cell mediated”, “delayed type”
o T cell mediated
o Classic examples:
• The tuberculin skin test (Mantoux test) – a positive reaction peaks 48 hour after injection of antigen
• Contact dermatitis - poison oak/ivy rash
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Type IV Hypersensitivity Reaction
Type IV is involved in pathogenesis of many auto immune and infectious diseases.
o Tuberculosis, Histoplasmosis, Rheumatoid arthritis (?)
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Primary immunodeficiency
Caused by abnormalities in development or function of T and/or B cells, (and / or of the granulocytic series)
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Primary immunodeficiency
o May be congenital, spontaneously acquired, or iatrogenic (caused by treatment by medical providers)
o Patients typically demonstrate unusual susceptibility to infection, increased occurrences of autoimmune diseases, and higher rates of lymphoreticular malignancies
o Disease are classified by mode of inheritance and whether the defect affects T cell or B cells or both
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Primary immunodeficiency
Selective IgA deficiency – the most frequently occurring primary immunodeficiency (1:500-600)
o Most are asymptomatic because of increase IgG and IgM secretion as a compensatory mechanism.
What symptoms might you see?
Recurrent sinusitis, otitis, bronchitis; usually diagnosed in young adulthood
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Primary immunodeficiency
Severe Combined Immunodeficiency (SCID) – rare; there is gross functional impairment of both humoral and cell-mediated immunity. Patients susceptible to devastating fungal, bacterial and viral infections and die in infancy from infection
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Primary immunodeficiency
X-linked agammaglobulinemia (XLA) (Bruton agammaglobulinemia) -rare
o Males begin to have recurrent bacterial infections in the first year of life after maternally derived immunoglobulin have disappeared.
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Secondary Immunodeficiency
Those immunodeficiencies not caused by abnormalities in development or function of T and B cells.
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Secondary Immunodeficiency
o Examples:
• AIDS –T cell may develop and function normally, but the over all number of T cells is very low
• Immunodeficiency related to malnutrition
• Immunodeficiency related to x-rays, immunosuppressive drugs
• Decreased production, or production of a less active cytokine such as granulocyte-colony stimulating factors (G-CSF) which results in neutropenia
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Secondary Lymphoid Organs
There are thousands of lymph nodes scattered throughout the body. They serve as hubs for incoming lymph vessels and the lymph (tissue juice) they contain. T cells, B cells, antigen presenting cells, and antigens travel through these areas in the small volume of lymph, making the probability that they will interact to efficiently activate the adaptive immune system
The spleen acts in a similar manner “filtering” the blood
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Comparison of Innate and Adaptive Immune Systems
In the innate immune system, the players are already in place to defend against relatively small quantities of invaders we meet on a daily basis. This system can be overwhelmed and the adaptive immune system comes into play. It is able to handled huge quantities of almost any invader, but it takes time to make the custom weapons it uses.
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Comparison of Innate and Adaptive Immune Systems
The innate system is responsible for sensing danger and activation of the adaptive immune system. It is much less “focused” than the adaptive immune system, responding to invasion
