H‐2: Its Structure and Similarity to HL‐A

Snell, George D.; Cherry, Marianna; Démant, Peter

doi:10.1111/j.1600-065x.1973.tb00108.x

Cited by 18 publications

(37 citation statements)

References 38 publications

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“…The unusual distribution of the genes for the H-2.28 and H-2.1 families of public specificities among murine H-2K and H-2D regions discussed by Snell et al (33,34) and D~mant et al (31) also deserves comment in this connection. It seems that the H,2.28 and H-2.1 specificities are never both coded in the same H-2K or H-2D region, but either one or the other is invariably present (31,33,34). This raises the possibility that an H-2.1-bearing molecule serves a similar function in other mouse strains to that ascribed to D' in the present experiments with BALB/c.…”

Section: Discussionmentioning

confidence: 99%

“…In the case of products of the H-2D d region, this structure is apparently embodied in a second molecule (D') that does not bear private H-2 specificities, but can be identified by antibodies in anti-H-2.28 sera (21,23,31,32). The unusual distribution of the genes for the H-2.28 and H-2.1 families of public specificities among murine H-2K and H-2D regions discussed by Snell et al (33,34) and D~mant et al (31) also deserves comment in this connection. It seems that the H,2.28 and H-2.1 specificities are never both coded in the same H-2K or H-2D region, but either one or the other is invariably present (31,33,34).…”

Section: Discussionmentioning

confidence: 99%

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Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Blanden¹,

McKenzie²,

Kees³

et al. 1977

The Journal of Experimental Medicine

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The T(c)-cell response to ectromelia virus infection was studied in BALB/c-H-2(db) mice which carry a loss mutation in the H-2D region that results in the absence from cell surfaces of a molecule (D') bearing certain public H-2 specificities. When infected, these mice showed a poor response of T(c) cells that recognize H-2D(d) plus virus-specific determinants on infected macrophage targets, but gave a normal response to H-2K d plus virus-specific antigens. However, their own infected macrophages do display wild-type antigenic patterns involving virus and H-2D(d) since they were killed as efficiently as wild-type (BALB/c,H- 2(d))-infected cells by T(c) cells specific only for H-2D(d) plus viral antigens. When tested in vitro, infected BALB/c-H-2(db) cells stimulated a poor T(c)-cell response to H-2D plus virus-specific antigens, but stimulated a normal response (in comparison with infected BALB/c macrophages) to H-2K(d) plus viral antigens. Uninfected BALB/c-H-2(db) cells stimulated a normal T(c)-cell response to minor H antigens or trinitrophenyl in association with H-2D(d), thus suggesting that the defective response to infection may reside in a failure of the relevant H-2D(d) antigens of mutant cells to physically associate with viral antigens. Close association of viral and H-2D-coded molecules was also suggested by ability of specific anti-H-2K or -H-2D to partially block T(c)-cell-mediated lysis of infected targets. These results were interpreted to mean that H-2Dd-dependent, virus- immune T(c) cells recognized an antigenic pattern consisting of virus- specific and H-2D(d) determinants with the latter borne on an H-2D molecule carrying serologically-defined H-2D(d) private specificities. A second H-2D(d)-coded molecule (D') was not required for recognition and lysis by activated T(c) cells, but was apparently necessary for efficient stimulation of precursor T(c) cells, perhaps by promoting appropriate physical association of viral and H-2D(d) molecules.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Blanden¹,

McKenzie²,

Kees³

et al. 1977

The Journal of Experimental Medicine

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“…H-2.28 and H-2.1 are not simple serological entities, but complexes or families of several antigenic specificities with very similar strain distribution (10,16). They are present in both the K region and the D region products, and the product of each K region or D region allele is of either the H-2.28 or the H-2.1 type (6,10,16). Thus, both the K and D region products exhibit two types of "allelic" or mutually exclusive variation.…”

mentioning

confidence: 99%

“…One of these involves the private specificities, since usually each K or D region allele produces only one private specificity; the second involves the H-2.28 and H-2.1 families, since each K and D region allele produces either an H-2.28 or H-2. 1 specificity but never the two in combination (6,10). This pointed to the possibility that the specificities belonging to the two apparently separate allelic systems, i.e., the private specificities on the one hand and the H-2.28/H-2.1 specificities on the other hand, may actually be under the control of the different genes (17).…”

mentioning

confidence: 99%

“…Antisera against H-2.28 react with both the K and D region products of H-2.28-positive alleles (6,10) and cap H-2D molecules (17)(18)(19)(20) Eluates. Acid elution of antibodies absorbed specifically on lymphocytes was used (27) (15) and/or by immunofluorescence, using the differential redistribution method (14,18 Immunofluorescence Assay of Antibody-Induced Redistribution (Capping).…”

mentioning

confidence: 99%

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H-2.28, an alloantigenic marker allelic to H-2.1, is expressed on all three known types of H-2 molecules.

Démant¹,

Iványi²,

Néauport–Sautès³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

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Each allele at the K or D region of the H-2 complex produces two kinds of "allelic" or mutually exclusive antigenic characteristics: its unique private specificity and a public specificity(ies) of either the H-2.28 or H-2.1 family. The private specificities of the K and D regions are expressed on H-2K and H-2D molecules, respectively. The D region produces another molecule, H-2L, which lacks the H-2K and H-2D private specificity but exhibits the H-2.28 or H-2.1 specificity. We analyzed the expression of the H-2.28 determinants on H-2K, H-2D, and H-2L molecules. When an antiserum against H-2.28 is used to sensitize cells where it can react with only H-2K molecules or H-2D molecules, by subsequent elution antibodies against H-2.28 are recovered that can also react with H-2L molecules. Hence, determinants reactive with antibodies against H-2.28 are present on H-2L as well as on H-2K and H-2D molecules. The expression of the H-2.28/H-2.1 polymorphism on all three known types of H-2 molecules, without some obvious relation to the private specificities, suggests that the antigenic determinants of these two kinds of allelic systems (private in contrast to H-2.28/H-2.1) may be controlled by separate genes, even when they are expressed on the same molecule.

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The private specificity H‐2.4 and the public specificity H‐2.28 of the D region are expressed on two independent polypeptide chains

et al. 1977

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The antigenic specificities H-2.4 (private) and H-2.28 (public) in the H-2a haplotype are controlled by the D region of H-2 as defined by the available recombinants. In previous studies we have demonstrated by the antibody-induced redistribution method that the antisera against these specificities contain antibodies against at least two different polypeptide chains. We here report the results of the indirect immunoprecipitation of radiolabeled antigens after solubilization with Nonidet-P40. The antisera against the two specificities precipitated from such extracts two different and independent polypeptide chains, indicating that the products of the D region, as presently defined, comprise at least two different molecules. The molecular weight of both chains is approximately 45 000, which is similar to other molecules bearing private H-2 antigenic specificities. Consequently, the chromosomal segment presently defined by recombination studies as the D region, must contain another locus, controlling the second polypeptide chain which is detectable by anti-H-2.28 antisera, besides the H-2D locus which controls the polypeptide chain bearing the private specificity H-2.4 as well as most of the public specificities.

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H‐2: Its Structure and Similarity to HL‐A

Cited by 18 publications

References 38 publications

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

Cytotoxic T-cell response to ectromelia virus-infected cells. Different H-2 requirements for triggering precursor T-cell induction or lysis by effector T cells defined by the BALB/c-H-2(db) mutation

H-2.28, an alloantigenic marker allelic to H-2.1, is expressed on all three known types of H-2 molecules.

The private specificity H‐2.4 and the public specificity H‐2.28 of the D region are expressed on two independent polypeptide chains

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