Lymphocyte alloantigens of the horse. III. ELY‐2.1: a lymphocyte alloantigen not coded for by the MHC

Abstract

Summary A new polymorphic locus of the horse which has several unusual properties is described. The suggested name for the locus is ELY‐2. The gene product of one allele at this locus, designated ELY‐2.1, has been identified with antisera raised as a result of pregnancy. Antibody to ELY‐2.1 was first detected on day 55 after conception in the serum of a mare in first pregnancy. This early onset of antibody is similar to that seen for antibody to ELA antigens, and suggests that the source of the antigenic stimulus may be the tissue of the equine endometrial cups. The antisera identifying ELY‐2.1 are cytotoxic and kill all peripheral blood lymphocytes from horses carrying the antigen. ELY‐2.1 is a cell surface molecule expressed on lymphocytes, erythrocytes, and platelets. Other cell types have not been investigated. The overall phenotypic frequency of ELY‐2.1 in several horse breeds was 16 %. The ELY‐2.1 antigen is controlled by an autosomal, dominant gene which is not coded by the ELA region (the major histocompatibility complex of the horse), nor is it identical to the ELY‐1 locus, which codes for another cell surface alloantigen of equine lymphocytes. Stimulator cells carrying ELY‐2.1 did not induce proliferation of ELY‐2.1 negative responder cells in mixed cultures of horse lymphocytes. Attempts to raise alloantisera to other alleles of the ELY‐2 locus through immunization with lymphocytes were unsuccessful. It is possible that the alternate allele(s) does not code for a gene product which is expressed. The function and biochemical nature of the ELY‐2.1 molecule are unknown.

Factors influencing equine chorionic gonadotrophin production in the mare

“…This may be caused by the immunological responses, both humoral and cell-mediated, the mare mounts against paternally inherited Class I major histocompatibility complex (MHC) antigens expressed on the surface of the invading chorionic girdle cells, but not trophoblast of the allantochorion (Crump et al 1987;Donaldson et al 1990Donaldson et al , 1992Donaldson et al , 1994. Considerable quantities of complement fixing lymphocytotoxic antibodies are produced by the mare beyond about 45 days of gestation in response to these alloantigens (Bright et al 1978;Allen 1979;Antczak et al 1982;Kydd et al 1982;Antczak 1984) and an anamnestic response occurs in subsequent pregnancies by the same sire, with antibody titres rising higher and earlier in gestation . Likewise, a similar heightened response is observed in primigravid mares that have previously received skin grafts from a MHC-incompatible sire prior to mating (Crump et al 1987).…”

“…1982; Kydd et al . 1982; Antczak 1984) and an anamnestic response occurs in subsequent pregnancies by the same sire, with antibody titres rising higher and earlier in gestation (Antczak et al . 1984; Allen et al .…”

A comparison of lymphocyte antigen specificities in Norwegian and Swiss goats

“…In other species, analogues to this specificity have been described, e.g. the equine specificity ELY-2.1, the only known allele of a locus called ELY-2 (Antczak 1984). In the goat, we suggest that this antigen specificity be designated GLY-1.1 and the locus GLY-1.…”

Genetic control of immune responses to major histocompatibility complex antigens during equine pregnancy

“…The sire of the embryo carried Ely 2.1, a non-ELA lymphocyte antigen, in addition to ELA W2 (Antczak 1984), whereas the dam of the embryo and the recipient mare were negative for that antigen. Thus it was possible that the antibody produced by the recipient mare was directed against Ely 2.1.…”

“…irrespective of the mare that makes the response or the source of the W3-positive lymphocytes used in the assay, and it implies that there is a genetic component that influences the immune response to these antigens. Furthermore, in one primiparous mare in which a specific response to W3 was identified, antibody was not detected until Day 70, the latest onset encountered for alloantibody production in MHC-incompatible equine pregnancy (Antczak et a/ 1984). Thus, the equine MHC antigen ELA W3 appears to be a weak immunogen compared to ELA W1 or ELA W2.…”