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Pathology II > EXAM 2 Immune System > Flashcards

EXAM 2 Immune System Flashcards

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1
Q

Innate Immunity Definition

A
  • natural or native
  • ready to attack before infection occurs
  • first 6-12 hours of infection
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2
Q

Epithelial cells

A

block microbes

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3
Q

Phagocytic cells

A
  • neutrophils, monocytes/macrophages

- non specific, endocytosis

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4
Q

Dendritic cells

A
  • initiate the innate response
  • during adaptive, DC progenitors sense pathogens and travel from bone marrow to non lymph tissue. Pathogens signal for them to mature, mature has high MHC II.
  • Strong APCs
  • Develop tolerance to own immune system. Used for immunotherapies
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5
Q

NK cells

A
  • Early protection with activating/inhibiting receptors.
  • Infected cell will express less MHC I, inhibitory receptors on NK are not engaged, activated ligands are expressed.
  • NK is activated and infected cell is killed
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6
Q

TLR

A
  • Toll Like Receptors
  • found on phagocytes, dendritic cells, epithelial cells
  • cytoplasm, endosymal
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7
Q

Adaptive Immunity

A
  • acquired/specific
  • develops after exposure
  • more powerful than innate
  • B cells produce antibodies
  • 1-5 days after infection
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8
Q

B cells

A
  • humoral immunity/ antibodies
  • get help from antigen presenting cells that have MHC on them
  • Elimination of EXTRACELLULAR antigens
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9
Q

T cells

A
  • cell mediated immunity
  • T lymphocytes - effector T cells
  • Helper T produce cytokines
  • Cytotoxic directly kill via apoptosis
  • Elimination of INTRACELLULAR antigens
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10
Q

Generative lymphoid organs

A

Thymus for T cells and bone marrow for B cells

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11
Q

Peripheral lymphoid organs

A

Lymph nodes, spleen, mucosal, cutaneous lymphoid tissues

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12
Q

“naiive” B and T cells

A

have not encountered an antigen yet

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13
Q

Lymphocyte recirculation

A
  • most important for T cells - naiive T cells circulate through the peripheral lymphoid organs and effector T cells circulate to the site of infection.
  • B cells don’t do this because they produce antibodies that will get into blood and go to the infection site. B cells do not go anywhere.
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14
Q

CD

A

Cluster of differentiation - help T cells recognize antigen

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15
Q

CD8+

A
  • Cytotoxic T cells
  • Class I MHC
  • On all nucleated cells
  • Any cells in the body can become infected and needs cytotoxic T cell to kill it. Help cytotoxic T cells recognize antigen
  • Kill infected cell
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16
Q

CD4+

A
  • Helper T cell
  • Class II MHC
  • present in antigen presenting cells only (macrophages and dendritic cells)
  • Antigen presenting cells release cytokines which signals Helper T cells to grow and differentiate
  • Helps Helper T cells recognize antigen
  • Activate phagocyte to kill microbes
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17
Q

Cytokines role

A
  • innate - TNF, IL1, IFNs and chemokines
  • Adaptive- by T helper cells –> IL2 and IL17
  • Colony stimulating factors (CSFs) by marrow cells, stimulate hematopoiesis
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18
Q

Steps of Cell Mediated Immunity

A
  1. Dendritic cells capture microbial antigen from epithelia/tissues
  2. Transports them to lymph nodes
  3. In the process, dendritic cells mature and express MHC molecules and costimulators
  4. Naive T cells recognize MHC molecules
  5. T cells become activated, proliferate, and differentiate into effectors and memory cells
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19
Q

Steps of Humoral Immunity

A
  1. Naive B cells recognize antigens because of Helper T cells and other stimuli
  2. B cells are activated, proliferate, and differentiate into antibody secreting plasma cells
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20
Q

IgG

A
  • activate complement

- only one that can cross placenta.

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21
Q

IgM

A
  • Most prominent

- activate complement

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22
Q

IgA

A
  • mucosal immunity

- prevents passage of foreign substances into the circulation

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23
Q

IgE

A
  • mast cell and eosinophil activation

- allergies and parasites

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24
Q

Type of Hypersensitivity that deals with antibodies

A

I, II, III

NOT IV

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25
Type I Hypersensitivity (&steps)
Immediate Hypersensitivity (IgE) 1. allergy introduced 2. Helper T activated and stimulate B cells to make IgE (in genetically susceptible people) 3. IgE binds to Fc receptor on Mast Cell 4. Activated mast cell secretes mediators that cause rxn
26
Type I reaction
- immediate (0-1 hr after exposure) - vasodilation, vascular leakage, smooth muscle spasm - late phase - leukocyte infiltration, epithelial damage, bronchospasm
27
Type II Hypersensitivity (&steps)
Antibody-Mediated Hypersensitivity (IgG, IgM) 1. Opsonization/phagocytosis 2. Complement and Fc receptor mediated inflammation with antibodies 3. Complement activates, by products cause neutrophils/ROS/inflammation 4. Antibody-mediated cellular dysfunction
28
Autoimmune Hemolytic anemia
- Type II - Rh antigen - opsonization and phagocytosis of red cells - hemolysis, anemia
29
Graves
- Type II - TSH receptor - Antibody-mediated stimulation of TSH receptors - Hyperthyroidism
30
Acute Rheumatic fever
- Type II - streptococcal cell wall antigen, antibody cross-reacts with myocardial antigen - Inflammation, macrophage activation - Myocarditis, arthritis
31
Insulin-resistant diabetes
- Type II - Insulin receptor target - Antibody inhibits binding of insulin - Hyperglycemia, ketoacidosis
32
Pernicious anemia
- Type II - Intrinsic factor of gastric parietal cells are target - Neutralization of intrinsic factors, decreased absorption of VitB12 - Abnormal erythropoiesis, anemia
33
Type III Hypersensitivity (&steps)
- Immune Complex Mediated Hypersensitivity 1. Immune complex formation - antibodies are secreted into the blood and react with antigens, antigen-antibody complexes are formed 2. deposition - complexes are deposited into various tissues 3. Inflammation/tissue injury - about 10 days after antigen presented in blood -> fever, urticarial, arthralgia, LN enlargement, proteinuria
34
Systemic Lupus Erythematosus
- Type III - Nuclear antigen (circulating or planted in kidney) involved - Nephritis, skin lesion, arthritis
35
Reactive Arthritis
- Type III | - Bacterial antigens lead to acute arthritis
36
Type IV Hypersensitivity (&steps)
NO ANTIBODIES INVOLVED 1. CD4+ secrete cytokines that stimulate inflammation adn activate phargocytes 2. Other helper T cells recruit neutrophils and monocytes which leads to further inflammation and tissue injury 3. CD8+ directly kill tissue cells
37
Rheumatoid arthritis
- Type IV - Inflammation mediated by Help T cell cytokines; roles of antibodies and immune complexes? - Chronic arthritis with inflammation, destruction of articular cartilage
38
Type I DM
- Type IV - Antigens of pancreatic islet beta cells - T cell mediated inflammation, destruction of islet cells by cytotoxic T cell - chronic inflammation in Islets, destruction of beta cells, diabetes
39
Contact dermatitis
- Type IV - Various environmental chemicals such as poison ivy or oak - Inflammation mediated by Helper T cell cytokines - Epidermal necrosis, dermal inflammation, causing skin rash and blisters
40
Characteristics of Autoimmune Diseases
- Reaction to self-antigen or self-tissue - Primary or Secondary - Organ specific of systemic
41
Immunologic Tolerance
- The reason that we do NOT have autoimmune dz - autoimmune = lack of tolerance - "unresponsiveness to an antigen even though lymphocytes are exposed to that antigen"
42
Central tolerance
T and B cells will be killed via apoptosis if they are recognized as self. B cells go through receptor editing
43
Peripheral tolerance
- Escape central and get caught = suppression and may be reversible. - Deleted via apoptosis. - regulatory T cells are suppressed - less prevention of immune reactions against self antigens. Apoptosis for T cells
44
Anergy
- during peripheral tolerance. | - lymphocytes recognize antigens but are unresponsive due to lack of co-stimulating signals.
45
HLA gene
genetic susceptibility for autoimmune dz.
46
Gateways to autoimmune dz
- infection, tissue injury, and inflammation | - Entry of lymphocytes into tissues, activation of self-reacted lymphocytes, tissue damage
47
SLE pathology
- Systemic Lupus Erythromatosus - systemic AI dz. - Antinuclear antibodies (ANAs) bind to DNA, RNA, proteins and Smith (Sm) antigen. - deposition of immune complexes and binding of antibodies to cells and tissue = injury - elimination of self-reactive B cells and ineffective peripheral tolerance mechanism. - production of interferons amplifies response
48
SLE clinical features
**Butterfly rash**, photosensitivity, usually in young women
49
Sjogren Syndrome pathology
- systemic AI - results from lacrimal and salivary gland destruction - Most have rheumatoid factor (IgM autoantibody) w/o having rheumatoid arthritis. - CD4+ react to an unknown self-antigen --> aberrant activation of both cellular and humeral (T&B)
50
Sjogren Syndrome clinical features
- women 50-60 y/o | - dry mouth and eyes
51
Scleroderma pathology
- chromic AI, widespread vascular damage, fibrosis in the skin and organs (GI, kidneys, heart, muscles, lungs). - Unknown external stimuli and/or genetic susceptibility - Major T and B cell activation - All leading to an increase of extracellular matrix of proteins; fibrosis of the skin and parenchymal organs. - CONSTANT ISCHEMIA/REPAIR
52
Scleroderma clinical features
- cutaneous fibrosis, especially on antebrachium. - Raynaud's phenomenon. - dysphagia d/t esophageal fibrosis. GI malabsorption, intestinal pain and obstruction. - Pulmonary fibrosis - respiratory failure
53
Recognition of allographs
graft antigens are recognized by T and B lymphocytes d/t differences in HLA alleles
54
Rejection of allografts
T lymphocytes and antibodies against graft antigens are produced. Destroy tissue grafts
55
Mechanism of allographs
foreign HA histocompatibility molecules on the endothelium and parenchymal cells of transplanted tissues trigger hosts' immune system
56
Direct pathway
host T cells recognize donor HLA on APC derived from the donor. **dendritic cells most important**
57
Indirect pathway
Host T cells recognize donor HLA after processing and presentation on host APC **CD4+ most important**
58
Acute T cell mediated rxn rejection of solid organs
- within initial months after transplant | - cytokines secreted by the activated CD4+ - inflammatory reactions in the graft - activated macrophages - graft injury
59
Chronic T cell mediated rxn rejection of solid organs
vascular lymphocytes reacting against alloantigens - secrete cytokines - inflammation. Mostly vascular, same mechanism as acute
60
Hyperacute rejection
- antibody-mediated reaction - Recipient has been previously sensitized to graft antigen (blood transfusion, pregnancy) - Circulating antibodies binds to graft endothelial HLA with an immediate (mins to days) complement
61
Acute rejection
- Within days or months of transplantation, not previously sensitized to transplantation antigens - Antibodies formed by the recipient - cause graft vasculature injury by inflammation and cytotoxicity
62
Chronic rejection
Insidiously affect vascular components, unknown mechanism
63
Hematopoietic transplant
- Bone marrow transplantation - Using hematopoietic stem cells - Recipient is irradiated with or without chemo, to minimize rejection
64
acute GVHD
- days - weeks - Immunocompetent donor lymphs recognize host cells as foreignand induce T cell mediated injury - CLINICAL: host immune system, skin, liver, and intestine get affected
65
chronic GVHD
- Ongoing cutaneous and GI injury can resemble that seen in scleroderma - Recurrent and severe infection
66
Immunodeficiency during transplantation
- Due to lethal doses or irradiation/chemo - Opportunistic infection - Activation of previously silent infection
67
Primary immunodeficiency
- hereditary, manifest between 6mo-2yr | - Defects in innate OR adaptive immunities
68
Secondary immunodeficiency
Due to infections, malnutrition, immunosuppression, autoimmunity, irradiation
69
Most common Immunodeficiency syndrome
AIDS
70
HIV transmission
Sexual (blood/mucosal), parenteral inoculation, vertical transmission
71
HIV Life cycle
- GP120 on HIV binds with CD4 on cell wall - HIV RNA released - Reverse transcriptase RNA--> DNA - Assembled into viron and released with phospholipid bilayer of host cell
72
HIV Acute stage
- death of memory CD4+ T - Infection established in lymphoid and presented to T cells - Spread via blood - Partial control of viral replication - 2-4 weeks after infection. Flu-like
73
HIV Latent stage
- asymptomatic establishment of chronic infection | - virus is concentrated in lymphoid tissue with low levels of viral replication
74
AIDS
- HIV chronic - marked by decreased levels of CD4+ - Destruction of lymphoid tissues - prone to opportunistic illnesses - No Tx? 3 yr survival rate
75
AIDS Sx
- chills, fever, sweats, swollen lymph nodes, weakness, weight loss - CD4+ below 200 cells/mm

Pathology II (10 decks)

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