Chapter 32 Adaptive Immunity

What are the 3 major functions of the adaptive immune system?

Recognize non-self, respond to non-self, remember non-self

Effector response

Cells that put into action

Anamnestic response

Memory cells

What is different about the adaptive immune system

Takes longer to activate

B and T cells both have

Effector and memory cells

Which lymphocytes are a part of innate and adaptive immunity?

B and T cells

What lymphocytes are only a part of innate immunity?

NK cells

Are B cells continuously produced throughout life?

Yes

Do B cells all look different or the same?

Same (undifferentiated)

B cell process

CD34+ stem cells —> B cells —> mature in bone marrow —> circulate as naïve B cells —> activated by antigen in lymphoid tissues —> plasma cells —> secrete antibodies (humoral immunity)

What do mature B cells have on their surface?

IgM and IgG

Are T cells continuously produced throughout life?

No, finite production

T cell process

CD34+ stem cells —> bone marrow —> mature in thymus (primary lymphoid tissue) —> naïve unactivated T cells circulate in blood/lymph tissue —> antigen binds for activation + replication —> activated T cells —> helper T cells (TH) or cytotoxic lymphocytes (CTLs/TC) —> secrete cytokines

What do mature T cells have on their surface?

CD4 or CD8

Antigens

Antibody generators

Immunogen

Complex, large molecules that elicit an immune response

Haptens

Antigens that are too small to elicit an immune response on their own

Epitope

Binding site of antigen

Number

Valence - number of binding sites (epitopes) on antigen + antibody

Paratope

Binding site on an antibody

Avidity

Overall strength of an antibodyy

Affinity

Strength of binding on a single binding site on an antibodyy

Natural immunity

Acquired through normal life experiences and not induced through medical means

Artificial Immunity

Produced purposefully through medical procedures (also called immunization)

Active immunity

Person developing their own immune response to a microbe

Passive immunity

Person receiving immunity made by another person

Example of natural active immunity

Getting strep for the first time

Example of natural passive immunity

Maternal antibodies passed during breastfeeding

Example of artificial active immunity

Vaccinations

Example of artificial passive immunity

Immunoglobulin therapy or antiserum (antivenom)

Major histocompatibility complex (MHC)

Differentiates between self and non-self - T cells

MHC Class I (what is it, where, binds to, found in what kind of cells?)

Endogenous antigen processing (in cytoplasm), binds to CD8+ T cytotoxic cells, found in all nucleated cells (not rbc) - virally infected/mutated cells

MHC Class II (what is it, where, binds to, found in what kind of cells?)

Exogenous antigen processing, binds to CD4+ T helper cells, found in APC (antigen presenting cells - DC, macrophages, B cells)

T helper cells (TH)

CD4+ activated by antigen on MHC class II - release cytokines

Cytotoxic T lymphocytes (Tc)

CD8+ activated by antigen on MHC class I - identify and destroy infected, cancerous, or foreign cells using cytotoxins

What are the two pathways for cytotoxic T cells?

Perforin (cytolytic) and CD95 (apoptotic - process cell death)

Regulatory T cells (Treg)

Control/regulate other cells + suppress immune response to prevent a bold reaction

How do we get autoimmune diseases?

Bold reactions

T cell receptors (TCRs)

Recognize and bind fragments of antigens

Can T cell receptors be secreted?

No

Binding site of TCR

a and b gene

Can B cell receptors be secreted?

Yes

BCR binding site

light and heavy

T cell activation - first signal

MHC class II to TCR

T cell activation - second signal

B7 and CD28, if no second signal —> it is an anergic cell (functionally inactive)

T cell activation - third signal

Cytokine release (differentiates naïve T cell —> effector cell)

Staphylococcal enterotoxin A and B, toxic shock syndrome toxin, mouse mammary tumor virus, putative proteins from Epstein-Barr and rabies viruses are all

Superantigens (SAgs) that contribute to microbial pathogenicity

Superantigens (SAgs) are a type of

exotoxin, trick T cells into activation which causes cytokine storms and pyrogenic cytokines (fever inducing)

B cells differentiate into

Plasma cells that secrete antibodies

B cells have what receptors for specific antigens

Immonoglobulin receptors

Do BCRs require APC for presentation?

No

Each B cell has a BCR specific for one

epitope

B cell activation —>

Proliferation and differentiation into plasma cells

B cells can be activated with and without

T cells

B cells are activated which make

plasma cells —> antibodies (also immunoglobulin and BCR)

What are antibodies also known as

Immunoglobulin (Ig)

What does immunoglobulin serve as

BCR

Fab

Part of immunoglobulin that binds to antigen, 2 of them

What is Fab made up of

Heavy + light chain

Fc

Constant region - effector of immunoglobulin

What is Fc made up of?

Heavy chain

Antibodies can be used as an

opsonin

IgG (binding sites, affinity, avidity, highest what, activates, how many to activate, can cross?)

Monomer with 2 binding sites, high affinity, low avidity, highest serum immunoglobulin, activates complement pathway, 2 required to activated classical complement pathway, can cross placenta (natural passive immunity)

IgD (binding sites, part of, signals, how to know its mature?)

Monomer with 2 binding sites, part of BCR, signals B cells to start antibody production, IgD + IgM on surface tell its mature

IgM (binding sites, affinity, avidity, first in what, activates, how many to activate?)

Pentamer with 10 binding sites, low affinity, high avidity, first Ig in all immune responses, activates complement (one required to activate classical complement pathway)

IgA

monomers and diamers, Secretory IgA

IgE (lowest what, does what, what cell binds to what portion, activated to what?)

Lowest Ig serum level, opsonization, mast cells bind Fc portion, activated to release histamine)

Primary antibody response is the

first time you see pathogen

Lag/latent period in primary antibody response

May last days to weeks because it takes awhile to start making antibodies, no antibodies detectable in blood

Antibody titer

Antibody concentration is low in lag period for primary antibody response

Which immunoglobulin appears first and second in primary antibody response?

IgM then IgG (antibody class switching)

Secondary antibody response

Memory response, so doesn’t require T cell activation, so faster

Secondary antibody response is characterized as having

Shorter lag, more rapid log phase, longer persistent, higher IgG titer (concentration), production of antibodies with higher affinity

What is the basis of a vaccine

First exposed = primary antibody response, next exposure = secondary antibody response

True or false - antibodies directly lyse and kill infected cells

False, they DO NOT do this

What do antibodies do to mark as bad?

Neutralization, opsonization, immune complex formation

Toxin neutralization

Antitoxin, ingestion by macrophages

Viral neutralization

Complement component

Primary (congenital) immunodeficiencies

Born with it, from genetic disorder

Acquired immunodeficiencies

Gained during life

What are the primary congenital immunodeficiencies?

Chronic granulomatous disease, X-linked agammaglobulinemia, DiGeorge syndrome, severe combines immunodeficiency disease (SCID)

What is the acquired immunodeficiency?

HIV —> AIDS (less than 200 CD4 T cells per microliter of blood)