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Adaptive Immunity Patho Flashcards

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1
Q

What is the third line of defense

A

Adaptive/acquired Immunity

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2
Q

what are inducible responders?

A

lymphocytes and serum proteins
do not preexist in large numbers, are produced in response to infection

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3
Q

what is clonal diversity

A

lymphoid cells differentiate into specialized immunocompetant cells (specialized T/B cells)

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4
Q

how is clonal diversity generated?

A

lymphiod cells begin in bone marrow, migrate to primary/central lymphoid organs where they become immunocompetent (develop antigen specific receptors)

cells in thymus turn into T-cells, cells in bone marrow turn into B-cells

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5
Q

what are naive immunocompetent cells? where are they found?

A

immunocompetent cells can respond to antigens but are naive if have not encountered antigen - migrate to lymph nodes & spleen or enter circulation

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6
Q

what is clonal selection?

A

when lymphocyte is presented antigen from APC, immunocompetent B&T cells differentiate and proliferate into specialized effetor cells

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7
Q

What can T cells differentiate into during clonal selection?

A

T helper cells, T-regulatory cells, T cyctotoxic cells, memory T-cells

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8
Q

what do T helper cells do?

A

activate and regulate immune response

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9
Q

what do T regulatory cells do?

A

suppress inappropriate immune response

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10
Q

what do B and T memory cells do?

A

long lived cells (decades - lifetime) that can be quickly activated in event of second infection - speed up immune response

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11
Q

what is humoral immunity

A

antibodies circulating in blood defend against extracellular antigens (microbes, toxins)

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12
Q

what is cellular/cell-mediated immunity?

A

T-cyctotoxic cells defend against intracelluar pathogens (viruses)

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13
Q

what are the role of antigens?

A

small molecules found on the surface of microbes or infected cells, serve as target for antibodies and antigen receptors on B&T cells

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14
Q

what are the roles of APCs

A

process antigens and present them on cell surface via MHC to T-cells

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15
Q

What are the three APCs

A

macrophages, b-cells, dendritic cells

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16
Q

what is the most common circulating Ig?

A

IgG

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17
Q

which Ig is found in blood and bodily secretions?

A

IgA

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18
Q

which Ig is found in blood and bodily secretions?

A

IgA

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19
Q

What is the largest Ig

A

IgM - first produced in primary respnonse and part of BCR complex on B cells

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20
Q

what is the Ig responsible for allergic reactions & defense against parasites

A

IgE

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21
Q

what Ig is part of the BCR receptor on B cells

A

IgD and IgM

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22
Q

which Igs are found in low concentrations?

23
Q

what are the functions if Igs?

Study These Flashcards
A

NAP - neutralize, agglutinizing, precipitating

24
Q

what do Th1 cells do?

Study These Flashcards
A

cellular immunity

25
what do Th2 cells do?
humoral immunity
26
what do Th17 cells do?
inflammation
27
what do T regulatory cells (Treg) do
suppress immune response
28
what is the humoral immune response
production of antibodies
29
what is the cell mediated response
T cytotoxic cells
30
what is the structure of an antibody
two identical heavy and two identical light chains held together by noncovalent bonds. Has 2 Fab fragments with with antigen binding site called paratope and an Fc fragment that interacts non-specifically with inflammation mediators and B cells
31
what are T cyctotoxic cells
T cells activated when T cell receptors (TCRs) detect foreign intracellular antigens presented on MHC-1 molecules. They attack cells and destroy them directly
32
what is the primary humoral response
Upon exposure to antigen, B-cells begin to differentiate over a lag period of 5-7 days into plasma cells and B memory cells. Then a IgM response will occur followed by an IgG response of equal or less amount (created by plasma cells)
33
what is the secondary humoral immune response
upon repeated exposure to antigen, B memory cells rapidly differentiate into plamsa cells creating a large IgG reponse and IgM response similar in magnitude to primary response.
34
describe clinical use of antibodies
vaccines (both active and passive)
35
what is the difference between MHC-1 and MHC-2 molecules
MHC-1 (endogenous antigens) is expressed by all nucleated cells, any change in that cell attributable to infection results in foreign antibodies being presented by MHC-1 and flag cell for destruction. MHC-2 (exogenous antigens) is expressed only by APCs, coexpressed with MHC-1, activate adaptive immune response (lymphocytes)
36
What is clonal selection
differentiation and proliferation of T&B cells into specialized effector cells
37
what is involved with Tc cell clonal selection?
TCR & CD8 binds to MHC-antigen complex, activating production of cytokines
38
what is the role of natural killer cells
kill cells that do not have MHC-1 molecules
39
what can activate M1 phenotype macrophage
Th1, NK, CD8 Tc cells
40
what can activate M2 phenotype macrophage
IL-4 & 13, Th2 cells
41
describe active vs passive immunity
active - host response to infection, activates adaptive immune response, long lived passive - does not involve host reponse, short lived,
42
what are differences with fetal/neonatal immune function
poorly developed immune response (esp IgG), rely on maternal passive antibodies until about 6 months. Maternal antibodies disappear around 10 months
43
what is different in regards to aging individual's immune response
decreased t cell, specific antibodies, and b memory cells, increased autoantibodies (IgA & IgG esp)
44
what is lupus
chronic, multisystem, inflammatory disease characteried by production of large variety of autoantibodies against nucleic acids, erythrocytes, coagulation properties, phospholipids, lymphocytes, platelets and many others
45
what is tolerance in relation to humoral immunity
tolerance = state of immunological control to avoid detrimental immune response against own cells/tissues central tolerance = tolerance in primary lymphoid organs like thyroid and bone marrow peripheral tolerance = tolerance in secondary lymphoid organs like lymph nodes and spleen
46
what are common symptoms of lupus that can lead to diagnosis
-positive antinuclear antibody (ANA) -malar (butterly) rash on face -photosensitivity
47
what are pharmacological treatments for lupus
NSAIDS, steroids, antimalarial (hydroxychloroquine), immunosuppressive drugs, IV Ig therapy
48
what are non pharmacological treatments for lupus
avoid sun exposure, smoking cessation, balanced diet with Vit D & fish oil supplements, avoid saturated fat, avoid live vaccines if on immunosuppressants, avoid stress
49
what is rheumatic arthritis (RA)
chronic, systemic autoimmune disease involving many tissue and organs but particularly joints
50
how are joints affected by RA
synovial inflammation, joint swelling, ankylosis, destruction of cartilage inflammatory & immune response leads to leukocyte, macrophage, and neutrophil migration, enzymes released that degrade synovial tissue and cartilage
51
what are the most significant cytokines in RA
IFN-gamma, IL-17, TNF, IL-1, RANKL
52
what are risk factors for RA
variations in HLA genes increased age female smoking obesity low SES
53
what are clinical manifestations of RA
-inflammation (fever, fatigue, weakess, anorexia, weight loss, aching, stiffness) -painful, tender joints - pain early on caused by swelling, later on caused by sclerosis of subchondrial bone and new bone formation, most commony metacarpophalangeal, proximal interphalangeal, and wrist joints -fever
54
what are 2 complications of RA
1. formation of cysts - can cause fistula 2. rupture of cyst or synovial joint both contribute to bone erosion and worse outcomes

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