Blood Group Systems and Immunohematology Theory
Foundations
Blood group antigens are inherited cell-surface structures catalogued by ISBT number; more than 40 systems exist, but ABO and Rh cause most clinically significant reactions. Know the genetics: ABO (chromosome 9) with H antigen (FUT1) as precursor; group O carries H only; A1 transferase is more efficient than A2, and weak subgroups (A3, Ax, Ael, B3, Bm) create forward/reverse discrepancies. Secretor status (FUT2) determines soluble A/B/H in secretions and shapes the Lewis phenotype through adsorption of plasma Lea/Leb onto red cells.
Rh: RHD and RHCE at 1p36; you must recognize both Fisher-Race (DCE) and Wiener (Rh-Hr) nomenclature. No d antigen exists. Distinguish weak D (reduced antigen density; types 1, 2, 3 rarely immunize) from partial D (missing epitopes; can make anti-D). The G antigen usually accompanies D and C. Other systems to know: Kell (K is highly immunogenic; anti-K suppresses erythropoiesis), Duffy (Fya/Fyb, the malaria receptor, often absent in people of African ancestry), Kidd (Jka/Jkb, complement-fixing, notoriously evanescent, causes delayed hemolytic reactions), MNS (M/N, S/s, U), and the Lutheran, Diego, Colton, Dombrock, Scianna, and Xg systems plus high-incidence antigens such as Vel.
Antibody behavior
IgM antibodies (ABO, Lewis, P1, M/N) are called naturally occurring, react at room temperature or immediate spin, agglutinate saline-suspended cells, fix complement, and rarely cause HDFN. IgG antibodies (Rh, Kell, Duffy, Kidd, S) are immune-stimulated, react at 37 C or AHG, cross the placenta, and mediate hemolytic transfusion reactions and HDFN. Enzyme treatment enhances Rh, Kidd, Lewis, and P1 reactivity and destroys Duffy, MNS, and Xg, a useful fingerprint for identification.
Rule of thumb: only an IgG antibody reacting at 37 C or AHG is clinically significant; if the patient's own cells express the antigen, that alloantibody cannot be present.