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• MNSs System


  • Discovered by injecting animals with human red cells
  • Antigens are M, N, S, & s
  • Antibodies – naturally occurring (IgM)
  • Anti-S and Anti-s commonly developed immune characteristics (IgG class) as a result of pregnancy or transfusion
• P System


  • Discovered by injecting animals with human red cells
  • Antigen: P1 is common
  • Antibody: Anti-P may be naturally occurring, most often an IgM antibody
• Lutheran (Lu) System


  • Antigens: Lua and Lub
  • Lu(a) negative phenotype is very rare
  • Antibodies: IgG
• Kell System


  • 4 antigens: K (Kell) & k (cellano), & Kpa & Kpb
  • Kp (a+) phenotype & Kp (a-b-) phenotype are both rare
  • Knull phenotype K– k– Kp (a-b-): associated with chronic granulomatous disease (CGD), an inherited defect in the anti-bacterial capacity of neutrophils
  • Antibodies: IgG
  • Kell antigens are important in transfusion medicine, autoimmune hemolytic anemia, & hemolytic disease of the newborn
• Lewis System


  • Antigens: Le a & Le b
  • Not an integral part of the red cell membrane, but are soluble antigens present in body fluids & secretions
  • Adsorbed onto the surface of red cells if they are present in the plasma in sufficient amounts
  • 3 phenotypes: Le (a–b–); Le (a+b–); & Le (a–b+)
  • Most common: (Le a+, Le b–)
  • Lewis phenotypes may change during pregnancy
  • Antibodies: only found in Le (a–b–) individuals, almost entirely IgM
  • Never been implicated in HDN (hemolytic disease of the newborn)
• Link between the Lewis blood group & secretion of the ABO blood group antigens

  • Presence of fucosyltransferase converts the Lewis a antigen to Lewis b
  • People with Lewis a antigens are usually ABH non-secretors, and the presence of the Lewis b antigen makes a person a secretor
  • Lewis negative (Le a–, Le b–) can be either secretors or non secretors
• Genetic influences on the Lewis phenotype red cells


  • Le, H, se (Non–secretor, Le (a+b–))
  • Le, H, Se (Secretor, Le (a–b+))
  • le, H, Se (Secretor, Le (a–b–))
  • le, H, se (Non–secretor, Le (a–b–))
• Duffy Blood Group


  • Antigens: Fy a & Fy b
  • The only rare phenotype is Fy (a-b-), higher frequency in countries where there is a high incidence of Plasmodium falciparum malaria
  • Gives a degree of immunity to the disease because the malarial parasite requires Duffy antigens to enter the red cells
  • Duffy glycoprotein is a receptor for chemicals that are secreted by blood cells during inflammation
  • Also a receptor for Plasmodium vivax, a parasite that invades red blood cells and causes malaria
  • RBCs that lack the Duffy antigens are relatively resistant to invasion by P. vivax
• Clinical significance of Duffy antibodies

  • Almost exclusively IgG
  • Can cause transfusion reactions (antibodies against the duffy antigens Fya, Fyb, & Fy3)
  • IgM is rare
• Basic biochemistry of Duffy

  • Duffy glycoprotein is encoded by the FY gene, of which there are 2 main alleles, FYA and FYB
  • They are codominant, meaning that is the FYA is inherited from one parent and the FYB allele is inherited from the other , both gene products, Duggy Fya and Fyb antigens, will be expressed on the RBCs
• Expression of Duffy antigens

  • Endothelial cells that line blood vessels
  • Epithelial cells of kidney collecting ducts
  • Lung alveoli
  • Purkinje cells of the cerebellum
  • Thyroid gland
  • Colon
  • Spleen
• Duffy phenotypes


  • Fy (a+b–)
  • Fy (a+b+)
  • Fy (a–b+)
  • Fy (a–b–)
• Kidd (Jk) System


  • Antigens: Jka & Jkb
  • Phenotypes: Jk(a–b–); Jk(a+b–); Jk(a–b+); Jk(a+b+)
  • Jk(a–b–) is a rare phenotype
  • Antibodies: almost exclusively IgG
• McLeod Phenotype


  • Lack Kx, poor expression of Kell antigens
  • Abnormal cell morphology– acanthocytic
  • Hemolytic anemia with reticulocytosis, bilirubinemia, splenomegaly
  • Muscular Dystrophy
  • Cardiomegaly
  • CGD
• Diego Blood Group System

  • Di a and Di b
  • Chromosomes 17
  • Wr a and Wr b
  • Wd a, Rb a, and WARR
  • Antibodies: IgG
• Cartwright Blood Group System


  • Yt a; Yt b
  • Yt a Not well-developed at birth, opposite of Yt b
  • Antibodies: IgD
• Xg Blood Group System

  • Xg a
  • Expression: 89% of a female population; 66% of male population
  • Antibodies: IgG
• Scianna Blood Group System

  • Sc system: Sc1 (Sm), Sc2 (Bu), Sc3
  • Chromosomes 1
  • Antibodies: IgG
• Dombrock Blood Group


  • Do a, Do b, Gregory (Gy a), Holley (Hy), Joseph (Jo a)
  • Do antigens common in Blacks
  • Do (a–b–), also lack Gy a, Hy, and Jo a
  • Antibodies: IgG
  • Can cause acute to delayed HTR
• Colton Blood Group System

  • Co a, co b, Co 3 (Co ab)
  • Colton antigens: located on transport protein channel-forming integral protein (CHIP) which forms primary erythrocyte water channel
  • Disease association: Co (a–b–): monosomy 7; dyserythropoietic anemia
• Chido/ Rodgers


  • 9 ags: Ch1, Ch2, Ch3, RG1, RG2
  • Poorly expressed on cord cells
  • Null phenotype associated with autoimmune disease such as SLE, RA, Graves Disease, Psoriasis
  • Antibodies: IgG
• Gerbich


  • Antigens: Ge2, Ge3, Ge4, Wb, Ls a, An a, Dh a
  • Chromosome 2
  • Antibodies: predominantly IgG with IgM
  • Anti–Wb and anti–LS: naturally occuring
• Cromer


  • Cr a, Te a, Dr a, Es a, IFC, UMC, WES b, Tc b, Tc c, WES a
  • Found in serum, plasma, urine, platelets, WBC, placental tissue
  • Poorly expressed on cord RBC
  • Encoded on chromosome 1
  • Anti–CROM antibodies predominantly IgG1
  • Mild Tranx rx.
• Knops


  • Kn a. Mc Ca (McCoy), SI a, Yk a, Kn b
  • Depressed expression: SLE, Chronic cold agglutinin disease
  • Antibodies: IgG
• Indian Blood Group System (IN)


  • In a, In b
  • Chromosome 11
  • Antibodies: IgG
• Bg Antigens


  • Bg a, Bg b, Bg C
  • Increased in Bg antigens linked with IM leukemia, polycythemia, hemolytic anemia
  • Antibodies: IgG
  • No implications in HDN and HTR