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Lewis, I, P & Se
Lewis, I, P & Secretor Status
| Question | Answer |
|---|---|
| What does the Se gene enzyme make in secretions? | H-substance |
| Se (FUT2) adds L-fucose to D-galactose on the Type 1 chain, making soluble H-substance, the foundation for soluble A, B and Leb. | Se gene enzyme function |
| Which genotype is a non-secretor? | sese |
| What percent of the population are secretors? | 80% |
| Which body fluid does NOT contain secretor substances? | CSF |
| How is the Lewis (Le) gene inherited? | Dominant; le is an amorph |
| How is Lea formed? | Le enzyme adds fucose to the Type 1 precursor chain (GlcNAc) |
| Leb is made from which substrate? | H-substance (needs Se and Le) Se makes H-substance first; the Le enzyme then adds a second fucose to make Leb. Lea is NOT converted to Leb. |
| Se and Le enzymes compete for L-fucose. Which acts first and wins? | Se, which is more efficient |
| RBC phenotype of Le + sese? | Le(a+b-) No H-substance means no Leb. Only Lea is made and it adsorbs to RBCs |
| RBC phenotype of Le_ and Se_ (adult)? | Le(a-b+) Leb out-competes Lea for the RBC surface |
| A person with lele has which RBC phenotype, regardless of Se? | Le(a-b-) No Le enzyme means no Lewis antigens. |
| Made in plasma/tissues and adsorbed onto the RBC Lewis antigens are soluble and ride on lipoproteins, then adsorb onto RBC glycolipids. Analogy: hitchhikers. | Lewis antigens |
| What Lewis type do all neonates/cord cells type as? | Le(a-b-) Cord cells are Le(a-b-) regardless of genotype. |
| Correct sequence of Lewis development in a Le+Se child? | Le(a-b-) → Le(a+b-) → Le(a+b+) → Le(a-b+) The true Le(a-b+) phenotype is reached by about 6-7 years. |
| A pregnant patient who was Le(a-b+) now types Le(a-b-). Why? | Transient loss of Lewis antigens during pregnancy Pregnancy causes a temporary Le(a-b-) type. |
| What are the usual class and temperature range of Lewis antibodies? | IgM, room temp/cold |
| Can a Le(a-b+) person make anti-Lea? | No, Lea is in their secretions Both Lea and Leb substances are in their secretions, so they are tolerant. |
| Do Lewis antibodies cause HDFN? | No; they are IgM and neonatal RBCs are Le(a-b-) IgM does not cross the placenta, and cord cells lack Lewis antigens. |
| Which phenotypes can make anti-Leb? | Le(a-b-) and Le(a+b-) Le(a+b-) people (Le, sese) have no Leb in secretions, so they can make anti-Leb. Anti-Lea is more common and stronger than anti-Leb. |
| Why are Lewis antibodies usually safe for transfusion? | Donor plasma neutralizes them and Lewis antigens elute from donor RBCs |
| Secretor inhibition: a '0' (no agglutination) result means what? | Antibody neutralized; soluble antigen present Saliva antigen neutralizes the antibody, so it cannot agglutinate the indicator cells. Agglutination means no soluble antigen. |
| Linear Type 2 chains, strong on cord/infant RBCs | i antigen Analogy: little i is a straight rope; big I is a branched tree. The relationship is reciprocal. |
| Auto-anti-I (cold agglutinin disease) is associated with which infection? | Mycoplasma pneumoniae |
| Auto-anti-i (cold agglutinin disease) is associated with which infection? | Mononucleosis (EBV) |
| Which disease is linked to auto-anti-i? | Infectious mononucleosis Infectious mononucleosis (EBV) is linked to auto-anti-i. |
| Anti-I is interfering with testing. Best workaround? | Prewarming techniques Prewarming helps. Cold autoadsorption or cord cells (low I) also work. Enzymes enhance anti-I. |
| The P antigen (globoside) is the receptor for which pathogen? | Parvovirus B19 |
| Anti-P1 is neutralized by what? | Hydatid cyst fluid or pigeon egg white |
| The Donath-Landsteiner antibody is what? | IgG biphasic hemolysin (auto-anti-P) in PCH |
| An IgG that binds in the cold (phase 1) and the cells hemolyze when warmed to 37°C (phase 2). Analogy: it bites in the cold, bursts when warmed. | biphasic hemolysin (auto-anti-P) in PCH |
| Which chromosome carries A4GALT (P1PK system), and where is the GLOB gene? | Chr 22 and chr 3 P1PK (A4GALT) is on chromosome 22; GLOB (P antigen) is on chromosome 3. Chromosome 19 is the Lewis (FUT3) gene. |
| Which antibody in the p phenotype is clinically significant? | Anti-PP1Pk (anti-Tja), IgG/IgM and hemolytic p-phenotype individuals make anti-PP1Pk (anti-Tja), which is clinically significant and linked to early miscarriage. The phenotype is very rare. |
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MOrfCLS
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