Phosphorylcholine-specific helper T cells in mice with an X-linked defect of antibody production to the same hapten.

Kaplan, Ruth Benca; Quintáns, José

doi:10.1084/jem.149.1.267

Cited by 20 publications

(5 citation statements)

References 14 publications

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“…Although it is possible that this finding is a result of the expression of the CBA/N defect directly at the T-cell level, this seems unlikely for two reasons. First, F1 male T cells have been shown to express T15 idiotype in levels similar to those found in F1 female T cells (20). Second, similar results are obtained using helper T cells from mice depleted of B cells and circulating T15 idiotype by injections of anti-g chain antibody from birth.…”

Section: Discussionsupporting

confidence: 67%

“…The 30% of T 15 + idiotypic B cells activated would represent the frequency of T 15-positive precursors in the PC-binding B-cell pool. Alternatively, one could argue that F1 males do have a limited number of T15 recognizing helper T cells, whose activity might result from exposure to the T and B cells bearing the T15 idiotype found in these mice (20,21). The helper T cells derived from OVA-primed F1 female mice by themselves elicit very small anti-PC responses.…”

Section: Discussionmentioning

confidence: 99%

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Mice whose B cells cannot produce the T15 idiotype also lack an antigen-specific helper T cell required for T15 expression.

Bottomly¹,

Mosier²

1979

The Journal of Experimental Medicine

100

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The X-linked CBA/N defect in B cell function precludes an antibody response to phosphorylcholine (PC). Accordingly, (CBA/N X BALB/c)F1 male mice are unresponsive to PC and lack circulating immunoglobulin bearing the T15 idiotype characteristic of BALB/C anti-PC antibody. In contrast, (CBA/N X BALB/c)F1 female mice respond to PC and greater than 80% of the anti-PC antibody is T15+. No T-cell abnormalities are known to be associated with the CBA/N mutation. These experiments compared the ability of helper T cells from either (CBA/N X BALB/c)F1 male (T15-) or F1 female (T15+) mice to help F1 female B cells respond to PC and to influence the level of T15 expression. The results indicate that although F1 male T cells collaborated with F1 female B cells just as efficiently as F1 female T cells for the total anti-PC response, the percentage of T15 expression induced by F1 male T cells fell dramatically. The (CBA/N X BALB/c)F1 male thus appear to lack a helper T-cell subset required for dominant idiotype production. This helper T cell defect could be repaired by adding F1 female T cells primed to a second carrier to F1 male T cells and restimulating the cell mixture with PC coupled to the antigen used to prime the F1 male cells plus free second carrier. This result implies that conventional helper T cells derived from the F1 male donor can collaborate with a distinct helper T-cell subset from the F1 female donor which recognizes both carrier and idiotype to induce an anti-PC antibody response dominated by the T15 clonotype.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Mice whose B cells cannot produce the T15 idiotype also lack an antigen-specific helper T cell required for T15 expression.

Bottomly¹,

Mosier²

1979

The Journal of Experimental Medicine

100

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“…The 7-day IgG anti-SRBC PFC responses of lethally irradiated Fi mice were measured after immunization with SRBC and reconstitution with anti-theta 4-C-treated spleen cells from normal Fi mice, along with the activated T cells as noted cell function known to be defective in xid mice is the ability of their T cells to augment LPS-induced B-cell activation (Goodman & Weigle 1979). Data indicating that the T cells of CD male mice are unable to support a T-15 predominant anti-PC response (Bottomly & Mosier 1978) have not been confirmed (Kaplan & Quintans 1979, Quintans et al 1981. Further studies are awaited to clarify this issue.…”

Section: Schermentioning

confidence: 99%

CBA/N Immune Defective Mice; Evidence for the Failure of a B Cell Subpopulation to be Expressed

Sche

1982

Immunological Reviews

113

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“…production, we found in another in vivo experiment that antibody titres to oxazolone were significantly higher in non-infected NK cell-depleted C57Bl/6 mice. In previous experiments investigating the importance of B cell function in S. aureus-induced septic arthritis, Zhao et al [10] have shown that expression of arthritis was less severe in Xid mice, which display disturbances of B cell functions [29], than in healthy controls. As these mice differed from the controls not only by showing lower levels of antibodies to S. aureus-specific antigens, but also in the total levels of immunoglobulin subclasses and as well as in spleen cytokine mRNA expression, it is not possible to point out a single B cell-dependent arthritis accelerating factor present both in the Xid and in our NK cell depletion model.…”

Section: Discussionmentioning

confidence: 99%

Protective role of NK1.1+ cells in experimentalStaphylococcus aureusarthritis

Nilsson

Bremell

Tarkowski

et al. 1999

Clinical and Experimental Immunology

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SUMMARYIn a model of Staphylococcus aureus-induced septic arthritis in C57Bl/6 mice we investigated the role of natural killer (NK) cells in the development of disease. Depletion of NK1.1 þ cells was achieved by repeated injections of the PK136 antibody, whereas control mice received an irrelevant monoclonal antibody, O1C5.B2. Both groups of mice then received injections intravenously with 2 × 10 7 live S. aureus LS-1 secreting toxic shock syndrome toxin-1 (TSST-1). The mice were evaluated for 16 days with regard to weight, mortality and arthritis. Nine days after bacterial injection, 9/19 mice depleted of NK cells had developed arthritis compared with 1/17 in the control group (P ¼ 0·01). The experiment was repeated twice with the same outcome. NK cell-depleted and control mice displayed the same degree of histopathological signs of arthritis at day 16. Depletion of NK cells did not affect uptake of bacteria by phagocytic cells in vitro, or bacterial clearance in vivo. In NK cell-depleted mice there was a tendency to increased levels of antibodies to TSST-1, whereas total immunoglobulin levels were similar to those in controls. NK cell depletion of non-infected mice did not affect the magnitude of inflammatory response during the T cell-dependent cutaneous DTH reaction to oxazolone, or during granulocyte-mediated inflammation. However, specific antibody responses to oxazolone were greatly increased in depleted animals. In conclusion, our study demonstrates that NK cells protect against arthritis during S. aureus infection. This outcome does not seem to be due to an influence on bacterial clearance, but could be due to an interaction with the host anti-inflammatory mechanisms.

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Phosphorylcholine-specific helper T cells in mice with an X-linked defect of antibody production to the same hapten.

Cited by 20 publications

References 14 publications

Mice whose B cells cannot produce the T15 idiotype also lack an antigen-specific helper T cell required for T15 expression.

Mice whose B cells cannot produce the T15 idiotype also lack an antigen-specific helper T cell required for T15 expression.

CBA/N Immune Defective Mice; Evidence for the Failure of a B Cell Subpopulation to be Expressed

Protective role of NK1.1+ cells in experimentalStaphylococcus aureusarthritis

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