4 week 24 Flashcards
(41 cards)
1
Q
What are the components of the immune system? (3)
A
- Physical + Chemical Barriers
- Cells (leukocytes)
- Tissues: Lymphoid (bone marrow, thymus, spleen, lymph nodes, and tonsils)
2
Q
Central lymphoid tissue vs Peripheral lymphoid tissue?
A
- CENTRAL:
- Bone marrow = Source of hematopoietic stem cells, Leukocyte development (except for final maturation of T lymphocytes).
- Thymus = T lymphocyte development (Immature T lymphocytes migrate here from the bone marrow).
- PERIPHERAL:
- Collections of B cells, T cells, and macrophages that trap microorganisms and foreign particles + Expose them to leukocytes in high concentrations. Also, spleen and lymph nodes filter blood and lymph, respectively.
3
Q
What are the two major types of defenses?
A
- Nonspecific defenses (Innate immunity) – rapid
- Physical barriers
- Inflammation
- Phagocytes
- Fever
- Interferons
- Natural killer cells
- Complement system
- Specific defenses (Acquired immunity) – slower
- Humoral (antibodies)
- Cell-mediated immunity
4
Q
What is inflammation? What are its 5 steps?
A
- inflammation = accumulation of proteins, fluid, and phagocytes in injured/invaded area.
- Tissue injury: macrophages phagocytose anything foreign.
- Some cells release histamine + signalling molecules = vasodilation = enhanced blood flow (+defensive proteins).
- Clotting factors are brought in to prevent blood loss… heparin prevents local clotting and allows blood to continue to flowing.
- Leukocytes squeeze b/w epithelial cells.
- Eventually rid invading microbe and repair injury.
5
Q
T or F: Leukocytes = both neutrophils and monocytes
A
true
6
Q
Diff bw macrophages and neutrophils?
A
- Macrophages are better at trapping microbes
- Neutrophils trap a few then die and become nets to trap things
7
Q
Steps of phagocytosis (4)
A
- Attachment:
- Specific—damaged cells or protein-targeted cells
- Proteins = opsonins (coat microbe to make it yummier)
- Internalization:
- Takes approximately 0.01 sec
- Phagosome + lysosome = secondary lysosome
- Degradation:
- Lysosome enzymes degrade phagocytosed product
- Exocytosis:
- Elimination of some degradation products
8
Q
What do IL-1, IL-6 and TNF-alpha do?
A
- Act on bone marrow to stimulate production of leukocytes
- Act on liver—production of acute phase proteins (some act as opsonins)
- Act as endogenous pyrogens to cause fever (IL-1 and TNF-alpha)
- IL-1 also stimulates T and B lymphocyte proliferation and differentiation
9
Q
Activated phagocytes release cytokines triggering additional immune responses. What are the 2 types of cytokines?
A
- Interleukins (communicate between leukocytes: IL-1, IL-6)
- TNF-alpha
10
Q
What causes fever? What is the purpose?
A
- Cause: Pyrogens change the thermoregulatory set point in the hypothalamus (> 37.2 C)
- Purpose: ↑metabolic activity of host + inhibition of some pathogens
11
Q
Which is the first cell to exit the bloodstream during inflammation?
A
Neutrophils
12
Q
What are interferons?
A
- Proteins secreted by leukocytes and virus-infected cells
- Interferon alpha, beta, gamma
13
Q
Diff bw interferons alpha and beta vs gamma?
A
- Alpha and beta: Stimulated by viral nucleic acids – Kill host cells + induces neighbouring cells to resist viral infection
- Gamma: Secreted from active T cells and NK cells + inhibits viral replication. Also enhances phagocytosis by macrophages, boosts antibody production in B cells, helps activate NK cells and cytotoxic T cells, and inhibits cell division—defense against cancer
14
Q
What do NK cells do?
A
- Remove abnormal/infected cells
- Lysis by perforins (think “pores”)
- Virus identification not necessary
- Early defense against viruses and tumor growth
15
Q
What is the complement system?
A
- Plasma proteins that are involved in foreign cells lysis, especially bacteria
16
Q
Complement system: describe the classical vs lectin vs alternate pathway
A
- CLASSICAL: Antigen-antibody complex = Formation of C3 Convertase = Membrane attack complex (MAC) OR ↑ inflammation and ↑ chemotaxis acts as opsonin
- LECTIN: Mannose on bacteria = Membrane attack complex (MAC) OR ↑ inflammation and ↑ chemotaxis acts as opsonin
- ALTERNATE: Pathogen surface = Formation of C3 Convertase = Membrane attack complex (MAC) OR ↑ inflammation and ↑ chemotaxis acts as opsonin
17
Q
What occurs earliest in the process of local inflammation?
A
Release of histamine
18
Q
What are the 2 main types of specific immunity?
A
- Humoral immunity
- B cell mediated
- Involves secretion of antibodies by plasma cells
- Defends against bacteria, toxins, and viruses in body fluids
- Cell-mediated immunity
- T cell mediated
- Involves lysis of cells by cytotoxic T cells
- Defends against bacteria, viruses in body cells
- Part of reaction to transplants and cancer cell
19
Q
What are the characteristics of specific immunity? (4)
A
- SPECIFICITY: given B cell or T cell recognizes a specific portion (epitope) of an antigen
- DIVERSITY: individual B and T cells recognize different epitopes/antigens (induces B or T cell to proliferate and differentiate = clonal selection)
- MEMORY: responsible for more rapid and greater secondary immune responses
- SELF-TOLERANCE: any B/T cells that have antigen receptors against normal body cells are destroyed
20
Q
What are the 2 types of cells formed upon activation of B/T cells?
A
- Effector cells:
- Combat antigen that stimulated production
- Short-lived (e.g. plasma cells)
- Memory cells:
- Long-lived (e.g. memory B cells)
21
Q
Describe antibody structure
A
- 2 heavy chains
- 2 light chains
- Constant region— same within a class of antibodies
- Variable region— differs for different antibodies, gives specificity
- 2 antigen-binding sites
22
Q
What are the functions of antibodies? (5)
A
- Neutralization: block activity of pathogen
- Agglutination: pathogens are aggregated by antibodies
- Opsonization: coating
- Complement activation: results in cell lysis
- Enhanced NK cell activity
23
Q
Describe the key features + roles for the antibodies IgG, IgE, IgA
A
- IgG: MOST COMMON + crosses placenta – all 5 functions
- IgE: involved in allergies – neutralizes, agglutinates, and causes mast cells and basophils to release histamine
- IgA: crosses epithelial cells and is present in mucosal sites + breast milk – neutralizes and agglutinates
24
Q
activevs passive humoral immunity?
A
- Active: memory cells – longterm (natural = sickness, artificial = vaccines)
- Passive: antibody – shortterm (natural = breastfeeding, artificial = antibody vax)
25
What are the 3 types of T cells?
1. Cytotoxic T cells – kill infected/cancerous cells in a specific manner
2. Helper T cells – help to activate cytotoxic and helper T cells, B cells, NK cells and macrophages
3. Suppressor T cells (T regulatory cells) – suppress activity of B cells, helper T cells and cytotoxic T cells
26
How are T cells activated?
when the antigens are associated with self-proteins called: Major Histocompatibility Complex (MHC) molecules
27
Class I vs II MHC?
- Class I: found on the surfaces of all nucleated cells in the body, present fragments of proteins, made in the cells (e.g., cytotoxic T cells/ CD8+ T cells).
- Class II: found on dendritic cells + macrophages + activated B cells, present fragments of proteins produced in phagolysosomes (e.g., Helper T cells/CD4+ T cells)
28
Describe the immune response mediated by T lymphocytes (1)
- ACTIVATION OF HELPER T CELLS
- Macrophages + dendritic cells engulf foreign antigen
- Antigen is cleaved into fragments
- Fragments bind to MHC class II molecules and the complexes are transported to cell surface
- Helper T cell that binds with the antigen/MHC class II complex is activated
- Helper T cell proliferates and differentiates into helper T cells that secrete cytokines and memory helper T cells
29
Describe the immune response mediated by T lymphocytes (2)
- ACTIVATION OF CYTOTOXIC T AND B CELLS
- Viral proteins synthesized in host cells are cleaved and fragments are bound to MHC class I
- Antigen/MHC class I complex transported to cell surface
- Cytotoxic T cell that binds with the antigen/MHC class I complex is activated
- Interleukin 2 (IL-2) and other cytokines released from helper T cells further stimulate the specific cytotoxic T cell
- Specific cytotoxic T cell proliferates and differentiates into cytotoxic T cells that kill infected host cells and memory T cells
- Note: cytokines released from helper T cells also further stimulate activated helper T cells and B cells
30
Describe the immune response mediated by T lymphocytes (3)
- ACTIVATION OF CYTOTOXIC T CELLS
- Activated cytotoxic T cells release perforins that insert into plasma membrane of the host cell forming a pore
- Activated cytotoxic T cells also release fragmentins (granzymes) that cause the host cell to die by apoptosis
- Phagocytes engulf cellular debris
- Note: Some cancers and viruses inhibit production of class I MHC molecules, thereby protecting them from the immune system
31
What is NOT a characteristic of a helper T cell?
A) Releases cytokines like interleukin 2 (IL-2)
B) Releases perforin
C) Secrete cytokines that stimulate B cells
D) Matures in the thymus
B) Releases perforin
32
What is tissue typing?
- Matching HLA (MHC) molecules between transplant donor and recipient
- Note: must still suppress immune response of recipient with drugs or radiation pre-transplant (which makes them more susceptible to infections and cancer)
33
Describe what happens in allergies like Hay fever
- B cells may recognize the pollen (receptors bind to it)
- Plasma cells produce antibodies
- Antibody binds to mast cell and activates it… causes release of histamine vasodilation, capillary leaking, allergy symptoms
34
What is anaphylactic shock? What is the treatment?
- Massive release of histamine from mast cells throughout the body
- Vasodilation → decreased total peripheral resistance (TPR) → decreased mean arterial pressure (MAP)
- Treatment = epinephrine (Increases cardiac output and TPR → increased MAP)
35
Autoimmune diseases vs immunodeficiency?
- Autoimmune diseases: when immune system treats a part of self like a pathogen and immune response is induced against that part (insulin diabetes, lupus, MS)
- Immunodeficiency: weak or underactive immune system (SCID, Hodgkins disease, AIDS)
36
What is the role of stress in the immune response?
- Stress suppresses the immune system (i.e., decrease number of leukocytes and promotes anti-inflammatory activity)
- Synthetic cortisol can be used to treat inflammatory diseases
37
What is Rh factor?
- “+” = presence of Rh factor (D antigen) on RBC [dominant]
- “-” = lack the D antigen
38
What is the risk if a mother is Rh- with a fetus that is Rh+ ?
- Risk that mother will develop antibodies that will attack the RBC of the fetus, causing hemolytic disease of the fetus
39
Diff bw first vs subsequent pregnancy with Rh- mother and Rh+ fetus?
- FIRST PREGNANCY:
- During delivery, fetal RBC enter maternal circulation
- Mother mounts immune response against D antigen -- memory T and B cells
- SUBSEQUENT PREGNANCY:
- If fetal RBC cross the placenta and enter the mother -- she will produce anti-D antibodies that can cross the placenta and destroy the fetal RBC
- Causes hemolytic disease of the fetus
40
How is hemolytic disease prevented?
- anti-D antibodies (called RhoGAM) are injected into the mother during the first pregnancy and just after labour
- RhoGAM does not cross the placenta
- RhoGAM helps to destroy the Rh+ RBC before they trigger an immune response in the mother
41
As a child, Lucia who is Rh negative was mistakenly transfused with Rh positive blood. She is now expecting her first child with an Rh positive partner. Should her doctors be worried about her pregnancy?
Yes because she developed immunological memory to the D antigen as a child.
