BioSci Adaptive Immunity

What is the main function of the adaptive immune system?

Recognize specific foreign antigens and activate targeted immune responses

What features make the adaptive immune system unique?

Incredible diversity (millions of antigens) and long memory for faster future responses

What cells are involved in the adaptive immune response?

B cells, T cells, and antigen-presenting cells (APCs) like macrophages and dendritic cells

In what types of infections is the adaptive immune system especially important?

Exotoxin-mediated diseases (e.g., tetanus, diphtheria), encapsulated bacteria (e.g., pneumococci, H. influenzae), and viral infections

What is passive immunity?

Receiving preformed antibodies (immunoglobulins) from another person, providing temporary protection.

How can passive immunity be naturally acquired?

Through the placenta or breast milk—antibodies passed from mother to child

What are the pros and cons of passive immunity?

Pro: Immediate protection.
Con: Short duration—antibodies degrade, lasting only 1–2 months.

When is passive antibody therapy lifesaving?

In diseases caused by exotoxins like botulism or tetanus—treated with antitoxins.

What is convalescent plasma, and when is it used?

Plasma from recovered individuals, given to severe cases (e.g., Ebola, COVID-19) to help speed recovery.

Who else receives passive antibodies, and why?

Severely immunocompromised individuals, because they can’t make their own antibodies.

How are lab-made antibodies used therapeutically?

Used in targeted treatments, such as DMARDs for autoimmune diseases

How is active immunity acquired?

Through exposure to the organism—via disease, subclinical infection, or vaccination.

How does the onset and duration of active immunity compare to passive immunity?

Slower onset (7–10+ days), but longer-lasting protection

What is the difference between primary and secondary immune responses?

Primary: slower (7–10+ days).
Secondary: faster (~3 days) with greater antibody production due to memory

What cells mediate active immunity?

B cells (antibodies) and T effector cells

What are antigens?

Immunogens that specifically react with B and T cells—they generate antibodies

What makes an antigen immunogenic?

It must be foreign, large, and structurally complex

What is an epitope?

A specific part of an antigen that binds to B cell receptors (antibodies) or T cell receptors.

What does it mean if an antigen is multivalent?

It has multiple epitopes, allowing it to bind to different receptors.

How are antigens presented to T cells?

By antigen-presenting cells (APCs) using MHC molecules on their surface

What is the function of MHC molecules?

They hold and display antigens and identify cells as self.

What is the human version of MHC called?

Human Leukocyte Antigen (HLA)—unique to each person

What is MHC restriction?

T cells only recognize antigens presented on self MHC molecules

What receptors do T cells use to bind antigens on MHC molecules?

CD4 or CD8 receptors, depending on the MHC class.

What is the "Rule of 8s" in T cell-MHC interactions?

• CD4 × MHC II = 8 (CD4 T cells bind MHC class II)

• CD8 × MHC I = 8 (CD8 T cells bind MHC class I)

What is the structure of MHC class I?

One MHC alpha chain + β2-microglobulin

What is the structure of MHC class II?

Two MHC chains: one alpha and one beta, both anchored in the membrane.

Where is MHC class I found?

On all nucleated cells (except RBCs)

What does MHC I present, and to whom?

Intracellular antigens (e.g., from viruses, tumors) to CD8+ cytotoxic T cells

What is the immune response triggered by MHC I presentation?

Killing of virus-infected or tumor cells by CD8+ T cells.

Why is β2-microglobulin clinically relevant?

It's shed from cells and elevated in conditions like multiple myeloma, leukemias, lymphomas, and viral infections

Where is MHC class II found?

Only on antigen-presenting cells (APCs) and B cells.

What does MHC II present, and to whom?

Extracellular antigens (e.g., bacterial, fungal, protozoan) to CD4+ T helper cells

What cytokines activate T cells and start clonal proliferation?

IL-2 and IFN-γ produced by macrophages.

What results from CD4+ T cell activation?

Clonal expansion and initiation of antibody response to remove extracellular pathogens.

What causes autoimmunity at the cellular level?

Autoreactive B and T cells recognize self-antigens on self MHC and trigger an inappropriate immune response.

Why do autoreactive cells lead to autoimmunity?

They were not properly deleted, so they survive and attack self tissues.

What are MHCs called in humans, and what is unique about them?

MHCs are called Human Leukocyte Antigens (HLAs), and they are somewhat unique to each individual.

Why do people respond differently to the same pathogen?

Because different HLA types bind antigens differently, leading to varied immune responses

How many HLA haplotypes does each person inherit, and from whom?

Each person inherits 2 haplotypes—one from their mother and one from their father.

Why are there thousands of different HLA types among people?

HLA genes are highly polymorphic, meaning they have many variations

How are HLA genes expressed on cells?

HLA genes are codominantly expressed, so both maternal and paternal haplotypes are shown on each cell.

What is the chance that siblings share both or one HLA haplotype?

25% of siblings share both haplotypes; 50% share one.

What happens if donor HLA types don’t match the recipient’s?

The recipient's immune system will recognize the graft as foreign and attack it

Why does the immune system reject mismatched grafts?

Because foreign HLAs and antigens signal that the graft is not self

How can acute graft rejection be prevented?

By matching major HLAs between the donor and recipient.

Rank graft types from most to least likely to be accepted.

Autograft > Syngeneic graft > Allograft > Xenograft

What type of rejection is caused by minor antigens over time?

Chronic rejection.

Why is long-term immunosuppression needed even with matched HLAs?

Because minor antigens can still trigger immune responses that lead to graft loss

Why aren’t minor antigens tested before transplantation?

Their impact is unpredictable and difficult to screen for.

Why are immunosuppressants given after transplantation?

To prevent or slow graft rejection, especially from minor antigens.

What are two major risks of long-term immunosuppression?

Opportunistic infections and cancer.

How quickly does acute rejection occur without immunosuppressants?

Within 2 weeks.

What happens if a second allograft from the same donor is transplanted?

It’s rejected within 1 week due to immune memory.

What causes hyperacute rejection?

Preformed antibodies, such as anti-ABO and anti-Rh.

How can hyperacute rejection be prevented?

By matching donor and recipient blood types.

What are immunoprivileged sites, and why might grafts survive there without immunosuppressants?

Sites like the cornea lack immune surveillance to prevent damaging inflammation.

Can some transplant recipients eventually stop immunosuppressants?

Yes, if they develop tolerance to the graft.

What is the first step in treating hematopoietic malignancies like leukemia with transplantation?

Destroy the patient's hematopoietic cells using aggressive chemotherapy.

What replaces the destroyed hematopoietic cells in leukemia treatment?

Donor hematopoietic stem cells (HSCs).

What is the graft vs. malignancy effect?

Donor T cells attack and kill remaining cancerous cells by recognizing them as foreign.

What causes Graft vs. Host Disease (GVHD)?

Proliferation of graft T cells that attack host cells as "foreign."

What is a major complication of GVHD?

Severe organ dysfunction, overwhelming infections, and often death.

Who is most at risk for GVHD?

Immunocompromised transplant recipients.

How can GVHD be prevented?

Treat donor tissue with anti-thymocyte globulin to eliminate T cells

Fetuses are a “foreign” tissue in a host, but the mother remains ______ to this tissue.

tolerant

The ______ prevents maternal T cells from reaching the fetus.

placenta

T cells in the placenta are mostly ______, promoting immune tolerance.

Tregs

High levels of ______ cytokines near the fetus suppress immune responses, increasing infection risk

anti-inflammatory

In Rh incompatibility, maternal antibodies attack fetal ______, potentially causing miscarriage.

RBCs

What triggers antibody production in Rh- mothers during pregnancy?

Fetal Rh+ RBCs entering maternal circulation

What medication is given to Rh- mothers to prevent sensitization?

RhoGAM

RhoGAM is given ______ the mother makes antibodies.

before

B cells can differentiate into ______ cells that actively secrete large amounts of antibodies.

plasma

What type of B cell remains in the body to respond quickly upon re-exposure to the same pathogen?

Memory B cell

B cells develop from the ______ lineage in the ______.

lymphoid; bone marrow

How do B cells assist T helper cells?

By acting as APCs and presenting antigens via MHC II to CD4+ T cells

Antibodies bind to specific parts of antigens called ______.

epitopes

Antibodies produced by a single clone of B cells are called ______ antibodies.

monoclonal

What complement-mediated structure do antibodies help form to lyse bacteria?

Membrane Attack Complex (MAC)

Name two ways antibodies protect against infection besides lysis.

Neutralization and opsonization

After an infection, antibody concentrations rise for a few weeks and then ______.

decline

What immune cells are activated via Fc receptors in antibody-dependent cellular cytotoxicity (ADCC)?

NK cells

In ADCC, antibodies bound to a target cell trigger immune cells to ______ the target.

kill

What kind of response do antibodies enable upon second exposure to the same pathogen?

Memory response

What are the 5 classes of antibodies?

IgG, IgM, IgA, IgD, and IgE

What is the % breakdown of antibodies in serum?

75% IgG, 15% IgA, 9% IgM, 0.2% IgD, and 0.004% IgE in serum

______ is the first antibody made during primary immune responses

IgM

What structural feature gives IgM the highest avidity of any antibody?

It’s a pentamer with 5 arms (10 antigen-binding sites)

IgM is restricted to ______ due to its large size.

blood vessels

What two key immune functions is IgM especially good at?

Agglutination and complement activation

______ is the most abundant antibody and appears later with high specificity and affinity.

IgG

What makes IgG capable of crossing tissues and the placenta?

Its small, monomeric size

Name two major functions of IgG besides neutralization.

Opsonization and complement activation

IgG has ______ subtypes, named IgG1 through IgG4.

4

______ is the second most abundant antibody and is key to mucosal immunity.

IgA

Secretory IgA is a ______ joined by a J chain and a secretory component.

dimer

Where is IgA commonly produced?

Mucosal sites (GI, respiratory, GU tracts)

IgA is found in ______, ______, and ______ to help protect newborns and mucosal surfaces.

tears, saliva, breast milk

______ is the least abundant antibody and is involved in allergic and parasitic responses.

IgE