Effect of Anti-immunoglobulin Antisera on Homograft Rejection in Mice

Manning, Dean D.; Jutila, John W.

doi:10.1038/newbio237058a0

Cited by 17 publications

(7 citation statements)

References 8 publications

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“…This agrees with the recent observation of a lower number of antibody-forming cells in the spleen, lymph nodes, and gut of germfree mice treated neonatally with anti-/z (24). We have since reported that neither anti-# nor anti-~,l~,2 antisera are capable of altering the course of homograft rejection in mice, even in massive doses far in excess of those required to effect profound humoral suppression (25). We report here the extension of our studies to include mice treated initially as young adults and our investigations of the mechanism and extent of this type of suppression.…”

supporting

confidence: 77%

“…We have no information bearing on the question of suppression of thymus-derived cells involved in humoral antibody responses other than the indirect evidence afforded by the homograft studies reported previously (25). In that case we found absolutely no evidence of prolongation of survival of homografted skin resulting from the use of either anti-/z or anti-~,l~,2, even when the grafted animals were massively treated from the day of birth on through the entire rejection period.…”

Section: Resultsmentioning

confidence: 39%

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Immunosuppression of Mice Injected With Heterologous Anti-Immunoglobulin Heavy Chain Antisera

Manning

Jutila

1972

The Journal of Experimental Medicine

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Neonatal injection of mice with rabbit anti-µ antiserum has been shown to produce complete loss of direct and indirect plaque-forming responses to sheep erythrocytes as well as loss of serum IgM and severe depressions of all other serum immunoglobulins. Similar injection of anti-γ1γ2 or anti-γ1 antibodies effects a loss of the indirect response but induces relatively minor alterations in serum Ig levels. Delaying initiation of anti-µ treatment until young adulthood results in a somewhat diminished effect on plaque-forming responses and serum Ig levels but triggers the release of high serum levels of an aberrant µ-bearing protein. Anti-µ suppression of genetically thymusless mice indicates that at least part of the target cells for suppression are bone marrow derived. A working hypothesis for the maturation of humoral antibody-producing cell lines as it relates to these data is discussed.

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supporting

confidence: 77%

Section: Resultsmentioning

confidence: 39%

Immunosuppression of Mice Injected With Heterologous Anti-Immunoglobulin Heavy Chain Antisera

Manning

Jutila

1972

The Journal of Experimental Medicine

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“…Second, since there is no known antibody production to the minor antigens, we could evaluate the in vivo effect of the B cells themselves rather than that of their secreted products. Third, it should be possible to assess subtle differences in responsiveness that might have been missed with antigenically more disparate grafts (65)(66)(67). We found that there was no delay in the kinetics with which ~MT mice rejected the BALB.B grafts ( Fig.…”

Section: Resultsmentioning

confidence: 77%

Successful T cell priming in B cell-deficient mice.

Epstein

Rosa

Janković

et al. 1995

The Journal of Experimental Medicine

259

174

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SummaryB cells are an abundant population of lymphocytes that can efficiently capture, process, and present antigen for recognition by activated or memory T cells. Controversial experiments and arguments exist, however, as to whether B cells are or should be involved in the priming of virgin T cells in vivo. Using B cell-deficient mice, we have studied the role of B cells as antigen-presenting cells in a wide variety of tests, including assays of T cell proliferation and cytokine production in responses to protein antigens, T cell killing to minor and major histocompatibility antigens, skin graft rejection, and the in vitro and in vivo responses to shistosome eggs. We found that B cells are not critical for either CD4 or CD8 T cell priming in any of these systems. This finding lends support to the notion that the priming of T cells is reserved for specialized cells such as dendritic cells and that antigen presentation by B cells serves distinct immunological functions.

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“…For this purpose, the infection was followed in mice deprived of B-lymphocytes by the administration, from birth, of rabbit antiserum to mouse IgM. In such mice, there is selective impairment of B-cell development, leading to a pan-specific suppression of the synthesis of all classes of immunoglobulin (8, 14, 16), whereas T-cell function remains intact (8,15). The results reported herein have demonstrated that initial control of the parasitemia is relatively unaffected by lack of B-cell function, whereas the parasites cannot be eliminated from the blood under such conditions.…”

mentioning

confidence: 99%

Trypanosoma musculi infection in B-cell-deficient mice

Vargas¹,

Viens²,

Kongshavn³

1984

Infect Immun

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The course of infection with Trypanosoma musculi was assessed in mice deprived of B-lymphocytes by administration, from birth, of rabbit antiserum to mouse immunoglobulin M (IgM). Initial control of parasitemia leading to the first crisis and establishment of the plateau phase was unaffected by lack of Blymphocyte function, although multiplicative forms persisted throughout the infection in anti-IgM-treated mice, instead of disappearing after the first crisis as in intact mice. Elimination of trypanosomes after the second crisis was not observed in anti-IgM-treated mice, which maintained high numbers of parasites in the blood and peritoneal cavity, resulting in some mortality. A temporary reduction in parasitemia was achieved in anti-IgM-treated mice by transfusion of immune plasma. Immunodepression, as measured by splenic mitogen responsiveness, and splenomegaly were both observed in anti-IgM-treated as well as in intact mice, indicating that these features of murine trypanosomiasis are independent of B-lymphocyte function. Since in T. musculi infection parasitemia can be controlled initially but not eliminated in mice lacking B-cell function, the only crucial protection provided by antibody would appear to be in curing the infection after the second crisis.

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Effect of Anti-immunoglobulin Antisera on Homograft Rejection in Mice

Cited by 17 publications

References 8 publications

Immunosuppression of Mice Injected With Heterologous Anti-Immunoglobulin Heavy Chain Antisera

Immunosuppression of Mice Injected With Heterologous Anti-Immunoglobulin Heavy Chain Antisera

Successful T cell priming in B cell-deficient mice.

Trypanosoma musculi infection in B-cell-deficient mice

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