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THEMES > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

what do antigens react with

A
  • antibody molecules and antigen receptors on lymphocytes
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2
Q

Epitope

A

portion or fragment of antibodies made of 5-15 amino acids that reacts with antibodies and lymphocyte receptors

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3
Q

where is the MHC located

A

On the APC

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4
Q

MHC function

A

allows the T lymphocyte to recognize epitopes of the antigens and disciminate self from non self.

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5
Q

does the TCR recognize any epitope

A

No, only the one bound to the MHC

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6
Q

3 examples of APC

A
  1. Dendritic cells
  2. Macrophages
  3. B lymphocytes
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7
Q

2 functions of APC

A
  1. capture and process antigens and present them to T lymphocytes
  2. Produce signals required for the differentiation and proliferation of T lymphocytes
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8
Q

Antibodody function

A

remove extracellular microorganisms and toxins

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9
Q

What do B cells require for maturation

A

bone marrow stromal cells and their cytokines

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10
Q

what do CD4 lymphocytes express on their surface

A

CD4 molecules and TCRs

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11
Q

most effecient APC for activation of T lymphocytes

A

Dendritic cells

while other APCs can, they are less efficient

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12
Q

how is T cell diversity achieved

A

VDJ recombination with junctional diversity. with D in the Beta chain

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13
Q

T cell developmental stages - 5

A
  • released from the BM as progenitor cells
  • aim is to build the receptor
  • interacts with self antigens and differentiates into either CD4 OR CD8
  • released from the thymus, express alpha or beta. cd3 complex with co receptors = NAIVE mature T cell
  • T cells circulate in the blood and go to secondary lympoid tissues to bind APC
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14
Q

TCR vs antibody recognition

A

For TCRs, they specifically recognize peptide epitopes presented by MHC molecules. For antibodies, they recognize a wider range of epitopes (often on the surface of the whole antigen, this can be sugars, carbohydrates etc).

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15
Q

Implication of TCR recognition

A

Bc it recognizes a short sequence, it is sensitive to any changes in the AA

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16
Q

Why is T cell co stimulation important - 3 -RAN

A
  1. Needed for survival/proliferation
  2. To induce differentiation
  3. Cell-cell cooperation
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17
Q

what is tolerance in T cells

A

It is a process which prevents T cells from reacting to body’s own cells. Initially occurs in the thymus (central) or in the immune periphery (peripheral)

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18
Q

T regs

A
  • help maintain immune balance
  • have autoreactive T cell receptors
  • inhibit other cells with autoreactive T cell receptors in the immune periphery
  • use special molecules, like CTLA-4 and PD-1, to “shut down” or inhibit the activity of other T cells
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19
Q

Th1

A
  • Stimulated by IL-12 (from dendritic cells or macrophages).
  • Produce IFN-γ, which helps activate macrophages and is important for fighting intracellular pathogens (e.g., viruses, some bacteria).
  • More involved in cell-mediated immunity
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20
Q

Th2

A
  • Stimulated by IL-4 (often from other T cells or mast cells).
  • Produce IL-4, IL-5, and IL-13, which help activate B cells for antibody production and promote responses against extracellular pathogens (e.g., parasites).
  • More involved in humoral immunity
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21
Q

CD4+ cells become - 3

A
  • follicular
  • effector/ helper
  • regulatory/suppressor
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22
Q

CD8+ cells become

A

cytotoxic

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23
Q

Intracellular pathogens

A

live inside cells… viruses and bact (hiv/tb)

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24
Q

Extracellular pathogens

A

parasites (worms) some bact like streptococuss

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25
Q

Th1 deficiency and overactivity

A

def- myobact infect
over- crohns and RA

26
Q

Th2 dysregulation

A

leads to allergic disease (asthma or atopic dermatitis) and responds to helminth worms schistosoma

27
Q

Parasites and allergens

A

both trigger the same immune response

28
Q

Th17 deficiency and overactivity

A

def- mucocutaneous infections from yeast candida albicans
over- autoimmune disease

29
Q

candida albicans

A

fungus (yeast) that naturally exists in small amounts in the human body, particularly in the mouth, gut, and vaginal area. Under normal conditions, it doesn’t cause problems, but when the immune system is weakened or the balance of microorganisms is disrupted (e.g., due to antibiotics), Candida albicans can overgrow and cause infections.

30
Q

Tfh mutation and overactivity

A
  • mutation of gene encoding CD40L leads to hyper IgM syndrome and overactivity leads to autoimmune disease
31
Q

Immunoglobins fxn

A

IgM – First antibody made, strong in early infection
IgG – Most abundant, long-term immunity, crosses placenta
IgA – Found in mucosal areas (gut, lungs, saliva, breast milk)
IgE – Involved in allergies and parasite defense
IgD – Role in B cell activation (least understood)

32
Q

Hyper IgM syndrome

A

as M is the intial one activated, there always has to be a switch depending on what you are affected with at the time and this is bc M fully enough to fight off infections

33
Q

T regs

A
  • boosting activity help with transplant rejection and autoimmune diseases
  • Reducing activity helps in cancer immune therapy and chronic infections
  • Prevents graft rejection and graft-versus-host disease (GVHD).
34
Q

CD8 cells activation

A

by IL-2 cells from the Th1 cells and micgrate to the secondary lymphoid tissue. Then they will produce the cytokines: TNFa, TNFb, and IFNy

35
Q

CD8 T cells clinical relevance

A

immune deffense against viruses, intacellular parasites e.g Listeria monocytogens

36
Q

How cytotoxicity works

A
  • Granule exocytosis which mediates the release of perforins and lytic granules
  • Expression of the Fas ligand which activates the caspase pathway leading to cell death
  • Also recruits effector cells such as macrophages
37
Q

functions of the IS

A
  • Transfer the MHC-peptide complex to lymphocyes
  • Regulates lymphocyte activation
  • Directs the secretion of cytokines and lytic granules
38
Q

consequences of failed IS

A
  • T cell gets half a signal and this could result in T cell apoptosis or anergy
  • Anergy is when the T cell is non reactive or non regulatory and no longer stimulates a proper immune response
39
Q

Do B cells require an MHC

A

NO

40
Q

positive selection

A

whether the cell binds to MHC

41
Q

negative selection

A

whether the cell binds to self antigen

42
Q

Are Tregs solely in the immune periphery

A

No, a small subset can also be found in the thymus

43
Q

What is a B cell

A

a specialized lymphocyte that expresses a BCR on its surface and produces antibodies upon activation

44
Q

Gene splicing

A

The rearrangement of genes for gene diversity (UNIQUE SPECIFICITY)

45
Q

Antibody structure - YAT VC

A
  • Y shaped monor with two heavy chains and two light chains connected by disulphide or non covalent bonds
  • Additional S-S bond folds individual glycoprotein chains into disticnt globular domans
  • The hinge region is flexible and allows for the binding of numeroud antigens that are various distances apart
  • Variable Fab region has the first 110 amino acids and binds proteins, lipoproteinsa=, etc
  • Constant region Fc defines isotypes and binds to other cells to mediate Fc effector functions
46
Q

what is IgA associated with

A

secretory protein (sIgA)

47
Q

Mechanisms of B cells following antigen exposure

A
  1. Neutralization of microbes and toxins
    Opsonization and phagocytosis
    ADCC

complement activation
2. Lysis of microbes
Inflammation caused by neutrophils
Phagocytosis of microbes opsonized by complement fragments 3b

48
Q

Development of B cells - 5

A
  1. mature in the BM with the help of stromal cells and cytokines
  2. Pro B cells - heavy chain rearrangement
  3. Pre B cells - light chain rearrangement
  4. Immature B cells - express IgM. Undergoes selection to ensure tolerance
  5. Mature B cells - express IgM and IgD. Circulate in the blood and lymph
49
Q

Do B cells have positive and negative selection

A

no
they just eliminate cells that bind to self antigens

50
Q

Activation of naive B cells

A
  • B cells bind directly to antigens using their BCR
  • The antigen is presented to the MHC-II by the B cell
  • The Th cell recognizes the antigen (binds to cytokine receptor on B cell) and produces cytokines which activate the B cell
  • The B cell is proliferated and differentiates into antibody producing plasma cells
  • It also differentiates into memory B cells
51
Q

T cell Independant antigen structure

A
  • large carbohydrates and lipid molecules with repeating subunits
52
Q

TI-1

A

can serve as TLR

53
Q

TI-2

A

activate B cells by simultaneously crosslinking multiple BCRs

54
Q

Resulting molecules of TI antigens

A
  • natural antibodies are og IgM isotype
  • no memory B cells
55
Q

How B cells deal with exogenous antigens

A
  • free viruses, bacteria, protozoa, yeats, toxins
  • they get engulfed by the B cell through enodcytosis. The lysosome reacts with the proteosome and degraded into peptides by a series of proteases
56
Q

Cytokine function in B cells - PEES

A
  • Promote differentiation of B lymphocytes to plasma cells
  • Enables plasma cells to produce antibodies
  • E enable B lymphocytes to proliferate
  • Stimulate B lymphocytes to synthesize and produce antibodies
57
Q

what does clonal expansion entail

A
  • It has to do with the B cells proliferating and basically expanding, BUT the antigen doesnt just bind to any BCR but it binds to the one that fits/matches
58
Q

when B cells differentiate, what do they undergo

A

Infinity maturation through somatic hypermutation

59
Q

How long does it take for the naiive B cell to be activated

A

4-5 days

60
Q

A subsequent exposure to the same antigen results in - 3

A
  1. Antibodies are produced rapidly
  2. Produced in large amounts
  3. Produced for a longer period of time
61
Q

Primary response to antigen vs Secondary

A

5-10 days vs 1-3 days

62
Q

Vaccination

A

Many B cells migrate to the bone marrow and produce antibodies for months or years after the antigen has been eliminated

and this is so there is a quicker response to an infection? = YES THIS IS LONG TERM IMMUNITY

THEMES (6 decks)

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