SEROLOGIC EVIDENCE FOR ANTIGENS CONTROLLED BY THE <i>Ir</i> REGION IN MICE

Götze, Dietrich; Reisfeld, Ralph A.; Klein, Jan

doi:10.1084/jem.138.4.1003

Cited by 96 publications

(25 citation statements)

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“…The membrane molecules involved in these interactions could be H-2 antigens or alloantigens coded for by the H-2 I region (Ia antigens) (8), both of which have been demonstrated on membranes of T and B cells (14,(23)(24)(25)(26). If the antisera react with antigens on T cells, these cells may be unable to efficiently interact with B cells.…”

Section: Discussionmentioning

confidence: 99%

Immune Responses in Vitro

Pierce

Kapp

Solliday

et al. 1974

The Journal of Experimental Medicine

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Interactions among macrophages (M¢),1 T cells, and precursors of antibody-producing (B) cells in the presence of antigen, mediated by direct cell-to-cell contact(s) and/or by soluble factors elaborated by one or more of the cells, are essential for development of optimal plaque-forming cell (PFC) responses to "thymus-dependent" antigens such as sheep erythrocytes (SRBC) and random terpolymer of L-glutamic acid6°-L-alanine3°-Ltyrosine ~° (GAT) by mouse spleen ceils in vitro (1-4). Recent experiments have defined some of the genetic requirements for successful physiologic interactions among antigen and these cells. First, M~b and lymphoid cells (T and B cells) need not be syngeneic for successful generation of PFC responses; allogeneic M~ support the development of PFC responses by lymphoid cells which are comparable in magnitude to responses which develop in the presence of syngeneic M~b (4-6). Thus no known genetic restrictions appear to govern the interactions of MO with T cells and B cells in the development of antibody responses in the mouse. Second, physiologic cooperation between T and B ceils requires that the T cells be syngeneic or semisyngeneic with B cells at the H-2 complex (7, reviewed in reference 8). It has been shown that identity of certain membrane molecules encoded by the H-2 complex is required for antigen-activated T cells to be able to supply the appropriate "second" stimulus required to trigger antigen-activated B cells into cycles of cell division and differentiation into mature antibody-producing cells. These membrane molecules may be the H-2 antigens themselves or other molecules coded for by the K end of the H-2 complex (8). In addition to the mechanism of T-cell-B-cell interaction requiring physical contact between crucial membrane molecules on T and B cells, humoral factors produced by activated T cells may also act on the membrane molecules on B cells to

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Section: Discussionmentioning

confidence: 99%

Immune Responses in Vitro

Pierce

Kapp

Solliday

et al. 1974

The Journal of Experimental Medicine

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“…Finally, 11 HD subjects from Norway were also included in afflicted propositi studied. Duration of overt disease was estimated from the date of first recorded clinical symptoms and ranged from 1 to 28 yr. 115 blood samples from members of 31 families of HD patients were also studied. First-degree relatives were defined as parents, children, and siblings of probands with HD whereas second-degree relatives were twice removed from the proband (i.e., grandparents, uncles, aunts, cousins, nieces, and nephews).…”

Section: Introductionmentioning

confidence: 99%

Antibodies to human caudate nucleus neurons in Huntington's chorea.

Husby¹,

Li²,

Davis³

et al. 1977

J. Clin. Invest.

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A B S T R APrevalence of antibody reacting with neuronal cytoplasm was 3% in 60 normal controls and 6% among a wide variety of patients with diverse neurological disorders. However, one-third of 33 patients with Parkinson's disease showed presence of antineuronal antibody. Among patients with HD, a significant association was noted between duration of clinical disease greater than 7 yr and titers of antibody of 1:2 or greater (P < 0.001).When 115 family members of HD probands were tested, 30% of unaffected spouses showed presence of antineuronal antibody. 23.2% of first-degree relatives at risk for developing HD were also positive (P < 0.001). 10.5% of second-degree relatives showed presence of antineuronal antibody. These data may support an environmental or infectious factor somehow involved in the ultimate expression of HD.

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“…In contrast to the wide tissue distribution of the H-2K and H-2D major histocompatibility antigens, the Ia antigens have a restricted distribution with principal expression on subpopulations of T and B lymphocytes (2)(3)(4)(5)(6)(7)(8). The mapping of such important immune functions as mixed lymphocyte reaction, graft versus host reactivities, immune response control (It genes), and cell-cell interaction determinants to the I region has stimulated efforts to identify possible relationships between Ia determinants and these immune functions (9)(10)(11)(12)(13)(14).…”

mentioning

confidence: 99%

Effects of anti-Ia sera on mitogenic responses. II. Differential expression of the Ia marker on phytohemagglutinin and concanavalin A-reactive T cells.

Niederhuber¹,

Frelinger²,

Dine³

et al. 1976

The Journal of Experimental Medicine

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Genes mapping in the I region of the H-2 complex control a system of lymphocyte alloantigens (Ia) which are expressed on a subpopulation of T cells and on most B cells. Specific anti-Ia serum in the presence of rabbit complement removed the splenic T-cell subpopulation responsive to Con-A, but did not affect the response to phytohemagglutinin (PHA) or Leucoagglutinin. Antibodies specific for Ia, H-2K, or H-2D membrane antigens were used without complement to pretreat spleen cells. These antibody pretreated cells responded normally to Con-A and PHA.

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SEROLOGIC EVIDENCE FOR ANTIGENS CONTROLLED BY THE Ir REGION IN MICE

Cited by 96 publications

References 4 publications

Immune Responses in Vitro

Immune Responses in Vitro

Antibodies to human caudate nucleus neurons in Huntington's chorea.

Effects of anti-Ia sera on mitogenic responses. II. Differential expression of the Ia marker on phytohemagglutinin and concanavalin A-reactive T cells.

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