Potentiation of a primary in vivo antibody response by alloantisera against gene products of the I region of the H-2 complex.

Pierres, Michel; Germain, Ronald N.; Dorf, Martin E.; Benacerraf, Baruj

doi:10.1073/pnas.74.9.3975

Cited by 33 publications

(18 citation statements)

References 24 publications

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“…However, absorption experiments have not been performed to prove directly that the effects observed were related to anti-I-J antibodies contained in these sera. One can infer, however, from such absorptions performed in previous studies, that antibodies to I-J region determinants are the active material in these reagents (13,14).…”

Section: Potentiation Of the Primary In Vivo Response To Srbc By Antimentioning

confidence: 92%

“…It was thus appropriate to determine whether such antisera would also alter in vivo immune responses. We reported recently (13) that microliter amounts of alloantisera against I k and I # gene products were able to potentiate primary IgM and IgG in vivo plaque-forming cell (PFC) 2 responses to suboptimal immunogenic doses of sheep erythrocytes (SRBC) in A/J and BALB/c mice, respectively. The same immunopotentiating activity was observed with an anti-I-J k antiserum in A/J mice.…”

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confidence: 99%

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In vivo effects of anti-Ia alloantisera. I. Elimination of specific suppression by in vivo administration of antisera specific for I-J controlled determinants.

Pierres¹,

Germain²,

Dorf³

et al. 1978

The Journal of Experimental Medicine

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The helper and suppressor regulatory activities exerted on antibody responses by T lymphocytes are associated with subregions of the I region of the murine H.2 (major histocompatibility) complex. Using antisera defining Ia antigens, raised by immunization between congenic pairs of mice differing at the ! region, specific suppressor T cells (1, 2) and their soluble and mediators (3-5)have been shown to bear I-J subregion coded determinants, whereas certain helper (enhancing) factors and possibly helper cells possess I-A coded determinants (6, 7).i Analysis of the effects of such specific anti-Ia antisera on immune responses can, therefore, provide information concerning the regulatory functions of the various ! region products, This approach has been used in various model systems, and several investigators have reported marked inhibition of in vitro lymphocyte reactivity by distinct anti-la antisera (8-12). It was thus appropriate to determine whether such antisera would also alter in vivo immune responses. We reported recently (13) that microliter amounts of alloantisera against I k and I # gene products were able to potentiate primary IgM and IgG in vivo plaque-forming cell (PFC) 2 responses to suboptimal immunogenic doses of sheep erythrocytes (SRBC) in A/J and BALB/c mice, respectively. The same immunopotentiating activity was observed with an anti-I-J k antiserum in A/J mice. Further studies revealed that in vivo administration of the same anti-I-J k antiserum decreases tumor growth in A/J mice inoculated with a syngeneic methylcholanthrene-induced fibrosarcoma (14), known to elicit potent suppressor T-cell responses active in inhibiting antitumor immunity (15, 16). These observations raised the possibility that the potentiation of SRBC PFC responses observed with the anti-I-J k antiserum, *

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Section: Potentiation Of the Primary In Vivo Response To Srbc By Antimentioning

confidence: 92%

mentioning

confidence: 99%

In vivo effects of anti-Ia alloantisera. I. Elimination of specific suppression by in vivo administration of antisera specific for I-J controlled determinants.

Pierres¹,

Germain²,

Dorf³

et al. 1978

The Journal of Experimental Medicine

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“…Adult thymectomy and administration of small doses of Cytoxan or antisera directed at the IJ subregion of the major histocompatibility complex in the mouse have also been shown to eliminate suppressor T-cell functions both in vio and in vitro (33)(34)(35). Moreover, diminished suppressor cell function was associated with both enhanced antibody formation and the capacity to generate cytotoxic cells to modified self or syngeneic tumor cells.…”

Section: Reactivitymentioning

confidence: 97%

Direct evidence for loss of human suppressor cells during active autoimmune disease.

Strelkauskas¹,

Callery²,

McDowell³

et al. 1978

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

147

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These studies indicate that a regulatory subset of Iym0hocytes is missing in patients with juvenile rheumatoid arthritis but these patients have antibodies in their serum that react with normal T cells. This regulatory subset of T cells is, however, present in patients whose serum shows little or no reactivity with normal T cells. In addition, patients who are deficient in this regulatory subset of lymphocytes have siguificantly higher numbers of cells secreting Ig as measured by a hemolrtic plaque assay. The significance of these observations old: first, they represent a positive relationship among the loss of regulation, overproduction of immunoglobulin, and the presence of anti-T cell antibodies; and second, and perhaps of equal importance, is the indication that serum from patients with autoimmune diseases may give us a readil av'table reagent with which to dissect further functionally distinct subsets of normal T cells in man. Recent progress in murine systems has demonstrated that both the type and the intensity of the cellular and humoral immune responses can be regulated by a complex series of cellular interactions involving distinct subsets of lymphocytes (1)(2)(3). It has been shown that antigen triggers subpopulations of T lymphocytes capable of helping, amplifying, or suppressing other T-cell or B-cell responses (4, 5). The human T cell, like its counterpart in the mouse, expresses in vitro various functions including proliferation. in response to soluble and cell surface antigens, elaboration of mediators, activation by polyclonal mitogens, and cytotoxic activities (6). In man, it is now clear that regulatory T cells exist and can be defined by their functional properties in both normal (7-9) and pathologic states (10, 11). More recent data support the notion that T-cell help and suppression are mediated by different subpopulations of T cells bearing distinct Fc receptors (12) and cell surface antigens as defined by allo-and heteroantisera (13,14).We have previously shown that sera from four patients with juvenile rheumatoid arthritis (JRA) Patients. Records of all children who have attended the arthritis clinic at the Children's Hospital (Boston, MA) were reviewed. Only those children for whom a positive diagnosis of JRA was confirmed were included in the study (15). There were 30 children with this diagnosis. They were between 3 and 19 years of age and included 5 boys and 25 girls. The time interval between the onset of the disease and the time the blood sample was taken varied between a few weeks (4-6 weeks) and 16 years. The mode of onset was systemic in 3, monoarticular in 9, and pauci or polyarticular in 18. The criteria for classification as active disease or remission were based on objective findings by physical examination alone. Thus, children with at least one swollen joint were considered to have active disease, whether or not they had other physical abnormalities such as limitation of motion, signs of synovitis, or joint deformities. Patients in remission had normal results o...

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“…These effects include prolonged graft survival (14), regulation of immunity to tumors (15,16), inhibition of schistosome granuloma formation (17), potentiation of antibody responses (18), and inhibition of T-helper cell induction (19). More recently, haplotype-specific suppression of antibody responses to antigens under Ir gene control (4), and prevention of clinical EAE (5) have been accomplished with monoclonal anti-I-A antibody.…”

Section: Discussionmentioning

confidence: 99%

In vivo therapy with monoclonal anti-I-A antibody suppresses immune responses to acetylcholine receptor

Waldor

Subramaniam

McDevitt

et al. 1983

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

141

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A monoclonal antibody to I-A gene products of the immune response gene complex attenuates both humoral and cellular responses to acetylcholine receptor and appears to suppress clinical manifestations of experimental autoimmune myasthenia gravis. This demonstrates that use of antibodies against immune response gene products that are associated with susceptibility to disease may be feasible for therapy in autoimmune conditions such as myasthenia gravis.

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Potentiation of a primary in vivo antibody response by alloantisera against gene products of the I region of the H-2 complex.

Abstract: Mice were immunized intravenously with suboptimal numbers (3.5-5 X

Cited by 33 publications

References 24 publications

In vivo effects of anti-Ia alloantisera. I. Elimination of specific suppression by in vivo administration of antisera specific for I-J controlled determinants.

In vivo effects of anti-Ia alloantisera. I. Elimination of specific suppression by in vivo administration of antisera specific for I-J controlled determinants.

Direct evidence for loss of human suppressor cells during active autoimmune disease.

In vivo therapy with monoclonal anti-I-A antibody suppresses immune responses to acetylcholine receptor

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