Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n.

Pierce, Susan K.; Klinman, Norman R.; Maurer, Paul H.; Merryman, Carmen F.

doi:10.1084/jem.152.2.336

Cited by 22 publications

(19 citation statements)

References 31 publications

(45 reference statements)

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“…All stimulatory interactions require that both the T and B cells recognize the stimulating antigen, and that both determinants be on the same antigen molecule. In addition, the extensive irradiation is likely to eliminate most allogeneic stimulatory interactions (8).…”

Section: Discussionmentioning

confidence: 99%

The collaborative phenotype of secondary B cells is determined by T lymphocytes during in vivo immunization.

Speck¹

1982

The Journal of Experimental Medicine

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It is well established that the gene products of the major histocompatibility complex (MHC) 1 are important in allowing effective collaborative interactions between T and B cells in humoral immune responses. Results from several experimental systems have demonstrated that T cells are restricted to collaborating with B cells or macrophages derived from inbred murine strains that share genes within the I region of the MHC (1-2). Subsequent studies using bone marrow radiation chimeras have demonstrated that it is not the MHC identity between collaborating T cells and B cells per se that is crucial, but rather the ability of T cells to recognize antigen in the context of the MHC gene products of B cells or macrophages (3-7). These studies implied that T cells that are exported to the periphery have been selected to collaborate with B cells or macrophages of the thymus MHC type. However, several recent experimental results provide evidence that each T cell population is composed of a mixture of selfand allo-MHC-restricted immunocompetent T cells (8-13) and that the MHC restriction of T cells is a consequence of antigen priming (3,14). If antigen selection does play a role in establishing a self-MHC-restricted T cell population, this process may be reflected in the immune B cell population. Previous studies have demonstrated that nonimmune (primary) B cells and immune (secondary) B cells have different requirements for MHC recognition by antigen-specific collaborating T cells (8)(9)(10)15). Primary B cells are able to interact with MHC nonidentical T cells, whereas secondary B lymphocytes require some form of MHC recognition by collaborating T ceils. Thus, antigen-driven events appear to influence the MHC collaborative phenotype of B cell populations. In this report, experiments were conducted to determine if the acquisition of the observed MHC collaborative phenotype of secondary B cells is dependent upon the presence and participation of T cells during immunization. The B cell populations in congenitally athymic and conventional thymic mice were analyzed after immunization with the predominantly T-dependent antigen 2,4-dinitrophenylhemocyanin (DNP-Hy) and the predominantly T-independent antigen DNP-Ficoll. Results of these studies demonstrate that the characteristic MHC collaborative phenotype of secondary B cells is only acquired after T-dependent antigen immunization in the presence ofT cells. This is despite the fact that T-dependent and

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Section: Discussionmentioning

confidence: 99%

The collaborative phenotype of secondary B cells is determined by T lymphocytes during in vivo immunization.

Speck¹

1982

The Journal of Experimental Medicine

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“…Although such complex recognition is characteristic of T cell specificity, there have been reports that imunoglobulins can also be restricted to the recognition of certain antigenic determinants in the context of cell surface antigens (10,11). Similarly, although many studies have indicated that B cell stimulation need not be haplotype restricted (4,(27)(28)(29), a few recent investigations have implied that under certain conditions B cells may only be stimulated by antigen presented in the context of cells of an appropriate H-2 haplotype (12)(13)(14)(15).…”

Section: Discussionmentioning

confidence: 99%

Participation of the major histocompatibility complex in antibody recognition of viral antigens expressed on infected cells.

Wylie¹,

Sherman²,

Klinman³

1982

The Journal of Experimental Medicine

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The capacity of the antibody repertoire to recognize complex antigens on viral-infected cells was investigated at the level of monoclonal B cell responses. A majority of primary B cells responsive to PR8(H1N1)-infected H-2 syngeneic cells produced antibody that bound viral determinants only in the context of infected cells and not the isolated virion. An examination of the fine specificity of such antibodies revealed that most could be distinguished by a panel of cells infected with closely related heterologous H1 influenza strains. Indeed, most antibodies bound hemagglutinin determinants of PR8 exclusively, and few were broadly cross-reactive. An examination of the same antibodies for their recognition of cell surface antigens revealed that the majority recognized MHC-encoded antigenic determinants. Thus, most BALB.K (H-2k) primary B cells responsive to PR8-L919 (H-2k) cells produced monoclonal antibodies that bound PR8-antigens only in the context of H-2Dk-infected cells. Most C57BL/10 (H-2b) B cells responsive to PR8-EL4 (H-2b) cells produced monoclonal antibodies that bound PR8 antigens only in the context of H-2Kb-infected cells. These latter antibodies were further shown to recognize that H-2Kb molecule by virtue of their capacity to be discriminated by a panel of PR8-infected H-2Kb mutant cells. These findings demonstrate that much of the antibody repertoire is capable of highly specific complex recognition of viral antigenic determinants in the context of the appropriate MHC alloantigen.

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“…The authors concluded that nonresponder macrophages were able to present GAT to T cells as efficiently as responder macrophages were. Pierce et al (1980) reached a similar conclusion using an even more complex system of measuring the response to an antigen (DNP-GL0).…”

Section: Experiments Examining T-b Collaborationmentioning

confidence: 60%

What Causes Immunological Nonresponsiveness?

Klein

1984

Immunological Reviews

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Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n.

Cited by 22 publications

References 31 publications

The collaborative phenotype of secondary B cells is determined by T lymphocytes during in vivo immunization.

The collaborative phenotype of secondary B cells is determined by T lymphocytes during in vivo immunization.

Participation of the major histocompatibility complex in antibody recognition of viral antigens expressed on infected cells.

What Causes Immunological Nonresponsiveness?

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