Transplantation Immunology

Define the three types of transplants.

Syngeneic graft: between identical twins; Allogeneic graft: between genetically distinct individuals; Xenogeneic graft: between different species.

Describe the role of ABO antigens in blood transfusion.

ABO antigens are carbohydrate antigens on RBCs; mismatched transfusion leads to IgM‑mediated type II hypersensitivity causing acute hemolysis.

Describe the role of RhD antigens in transfusion reactions.

RhD is a protein antigen; anti‑D antibodies are IgG and can cross the placenta, causing hemolytic disease of the newborn; prevented with RhoGAM.

What causes an acute hemolytic transfusion reaction?

Recipient IgM antibodies bind donor RBC ABO antigens → complement activation → intravascular hemolysis within 1 hour.

Differentiate graft-versus-host disease (GVHD) from transplant rejection.

GVHD: donor T cells attack host tissues (skin, liver, GI). Transplant rejection: host immune system attacks donor graft.

What is graft-versus-host disease?

Donor T cells recognize host cells as foreign → type IV hypersensitivity → rash, jaundice, diarrhea, hepatosplenomegaly.

What is transplant rejection?

Host T cells and antibodies recognize donor alloantigens (HLA/minor antigens) → graft damage.

Identify the role of histocompatibility antigens in transplant rejection.

Major histocompatibility antigens = HLA mismatch; Minor histocompatibility antigens = polymorphic intracellular proteins; both trigger alloimmune responses.

What are alloantigens?

Foreign HLA + minor histocompatibility antigens that stimulate host immune rejection.

Compare hyperacute, acute, and chronic rejection.

Hyperacute: minutes; preformed antibodies; thrombosis/necrosis. Acute: weeks–months; host T cells attack donor HLA; vasculitis. Chronic: months–years; indirect allorecognition → fibrosis and arteriosclerosis.

Hyperacute rejection mechanism.

Preformed recipient IgG antibodies (anti‑HLA or anti‑ABO) bind graft endothelium → complement → thrombosis → ischemia.

Acute rejection mechanism.

Host CD8+ and CD4+ T cells recognize donor HLA via direct allorecognition → vasculitis; may also involve new antibodies.

Chronic rejection mechanism.

Indirect allorecognition → host APCs present donor peptides → CD4+ T cells and antibodies cause fibrosis and arteriosclerosis.

Why does Rh incompatibility cause disease but ABO incompatibility usually does not?

Anti‑D is IgG (crosses placenta); anti‑A/anti‑B are IgM (do not cross placenta).