Distribution of immunoglobulin isotypes in the nonspecific B-cell response induced by infection with Plasmodium chabaudi adami and Plasmodium yoelii

Langhorne, Jean; Kim, K.J.; Asofsky, Richard

doi:10.1016/0008-8749(85)90187-x

Cited by 24 publications

(13 citation statements)

References 22 publications

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“…IgGza and IgG2b PFC largely contribute to the total response while IgGl and IgG3 PFC remain poorly represented. These results confirm those obtained by J. Langhorn for P. chabaudi adami, a nonvirulent strain of this rodent malaria [4].…”

Section: Discussionsupporting

confidence: 91%

“…This contrasts with what occurs during infection with another strain of this parasite P. chabaudi adami. In this case, it has been shown that IgGl in absent in mice which recover from a primary infection [5] and that, indeed, Ig does not seem to play a role in protection since the passive transfer of immuneserum does not alter the course of infection [18]. Moreover, B cell-deficient mice can control the P. chabaudi adami infection [19].…”

Section: Discussionmentioning

confidence: 94%

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Isotypic pattern of the polyclonal B cell response during primary infection by Plasmodium chabaudi and in immune‐protected mice

et al. 1987

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The primary infection by P. chabaudi induces an increase of the numbers of splenic immunoglobulin (Ig)-secreting B cells in both athymic and euthymic BALB/c mice. The isotypic pattern of the polyclonal response is restricted only in euthymic mice where IgG2a, IgG2b and IgM plaque-forming cells (PFC) predominate. In immunized animals, protected against a parasite challenge, the isotypic pattern of splenic PFC is completely different, the IgG1 and IgM isotypes constituting the main part of the response. Reinoculation of immune-protected animals induces a PFC response which is dose dependent and accentuates the characteristic isotypic profile of the immune-protected mice.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 94%

Isotypic pattern of the polyclonal B cell response during primary infection by Plasmodium chabaudi and in immune‐protected mice

et al. 1987

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“…The overall strength of the B cell response could be misleading, because malaria is known to generate a large polyclonal B cell response (51,52). The kinetics of this response correspond well with the peak prevalence of Ab-containing cells in the infected spleens.…”

Section: Discussionmentioning

confidence: 99%

Plasmodium chabaudi chabaudi Infection in Mice Induces Strong B Cell Responses and Striking But Temporary Changes in Splenic Cell Distribution

Achtman¹,

Khan

MacLennan

et al. 2003

The Journal of Immunology

129

130

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B cells and Abs play a key role in controlling the erythrocytic stage of malaria. However, little is known about the way the humoral response develops during infection. We show that Plasmodium chabaudi chabaudi causes major, but temporary changes in the distribution of leukocytes in the spleen. Despite these changes, an ordered response to infection develops, which includes vigorous extrafollicular growth of plasmablasts and germinal center formation. Early in the response, the lymphocytes in the T zone and follicles become widely spaced, and the edges of these compartments blur. This effect is maximal around the peak of parasitemia. Germinal centers are apparent by day 8, peak at day 20, and persist through day 60. Extrafollicular foci of plasmablasts are visible from day 4 and initiate a very strong plasma cell response. Initially, the plasma cells have a conventional red pulp distribution, but by day 10 they are unconventionally sited in the periarteriolar region of the white pulp. In this region they form clusters occupying part of the area normally filled by T cells. B cells are absent from the marginal zone for at least 30 days after the peak of infection, although flow cytometry shows their continued presence in the spleen throughout infection. Relatively normal splenic architecture is regained by day 60 of infection. These results show that the changes in splenic cell distribution are linked to the presence of parasites and do not seem to interfere with the development of the humoral response.

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“…Malaria episodes are associated with raised concentrations of both specific and polyclonal of antibodies [20-22] and this may, in part, explain the reduced IgG1 antibody half-lives observed. However, in some children, the antibodies had extremely short half-lives suggesting that other processes, besides ordinary catabolism, may be contributing to the decay.…”

Section: Discussionmentioning

confidence: 99%

IgG antibody responses to Plasmodium falciparum merozoite antigens in Kenyan children have a short half-life

Kinyanjui

Conway

Lanar

et al. 2007

Malar J

165

151

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Distribution of immunoglobulin isotypes in the nonspecific B-cell response induced by infection with Plasmodium chabaudi adami and Plasmodium yoelii

Cited by 24 publications

References 22 publications

Isotypic pattern of the polyclonal B cell response during primary infection by Plasmodium chabaudi and in immune‐protected mice

Isotypic pattern of the polyclonal B cell response during primary infection by Plasmodium chabaudi and in immune‐protected mice

Plasmodium chabaudi chabaudi Infection in Mice Induces Strong B Cell Responses and Striking But Temporary Changes in Splenic Cell Distribution

IgG antibody responses to Plasmodium falciparum merozoite antigens in Kenyan children have a short half-life

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