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Rahul Saha: JAMA The 49th Human Blood Group System
Rahul Saha/LinkedIn
Sep 28, 2026, 03:59

Rahul Saha: JAMA The 49th Human Blood Group System

Rahul Saha, Pharmacokinetics (DMPK) and Clinical Pharmacology for Aera Therapeutics, shared a post on LinkedIn:

“Hello everyone.

Today I would like to post a comprehensive analysis on the ‘newly discovered 49th Blood Group System: JAMA’

JAMA is not a new ABO type blood group.

It is a newly ratified protein based blood group system defined by a single high prevalence epitope on junctional adhesion molecule A (JAM A).

In September 2026 the ISBT Working Party on Red Cell Immunogenetics and Blood Group Terminology recognised it as ISBT 049, the 49th human blood group system.

Most newly ratified systems, including JAMA, are protein antigens found by combining:

  • a pan reactive alloantibody that fails to react with the proposita’s own cells and with a close relative
  • whole exome sequencing (WES)
  • proof that the candidate protein is present on red cells and that the variant abolishes the epitope

Discovery: a pan reactive antibody and two siblings:

The index case was an Israeli woman whose plasma contained a moderately strong alloantibody that reacted with almost every red cell tested by indirect antiglobulin test (IAT).

Her own cells were non-reactive. So were her brother’s. That pattern points to absence of a high-prevalence antigen, not to a mixture of common specificities.

The wild type codon (c.644G) encodes p.Arg215 of JAM A.

That arginine defines the high prevalence antigen. The Gln215 protein is still produced; the substitution removes the epitope recognised by the patient’s antibody.

The antibody also bound platelets, consistent with the known expression of JAM A on both lineages.

F11R encodes a type I transmembrane glycoprotein of the immunoglobulin superfamily (IgSF), CTX subfamily.

Alternative 5′ UTRs and two promoters exist (type 1 transcripts in endothelium, platelets and leukocytes; type 2 more restricted to endothelium), but they encode the same mature protein.

The defining allele pair for the system is therefore:

  • Reference (antigen positive): F11R c.644G lead to p.Arg215
  • Rare antigen negative: F11R c.644G higher than A lead to p.Arg215Gln (homozygous in the two siblings)

This is a missense, epitope loss mechanism, not a null allele that deletes the protein.

ClinVar already lists c.644G higher A (p.Arg215Gln) among rare F11R missense variants; a neighbouring change, c.643C higher T (p.Arg215Trp), also exists.

Whether Trp215 also abolishes JAMA1 has not been published as part of the blood group work.

Structure of JAM A:

Mature JAM A is organised as:

  • Signal peptide (cleaved)
  • Extracellular region with two Ig like domains

A. D1 (membrane distal, V type): roughly Ser28 Lys125

B. D2 (membrane proximal, C2 type): roughly Pro135 Arg228

  • Single transmembrane helix
  • Short cytoplasmic tail (40 residues) ending in a type II PDZ binding motif (TSSFLV)

Disulphide bonds stabilise D1 (Cys50 to Cys109) and D2 (Cys153 to Cys212).

A single N glycosylation site sits at Asn185 in D2.”

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