Thymocytotoxic autoantibodies found in mice infected with Schistosoma japonicum

Kawabata, Masato; Hosaka, Yukio; Kumada, M.; Matsui, Norio; Kobayakawa, Takatoshi

doi:10.1128/iai.32.2.438-442.1981

Cited by 13 publications

(7 citation statements)

References 10 publications

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“…The nature of a signal(s) which induces CA as well as the ultimate fate of cortical thymocytes remains to be elucidated. Thymocytotoxicity by adrenocorticotrophic hormones or thymic antibody or both, in addition to increased emigration of cortical thymocytes to peripheral tissues, may all be considered (8,16,20). A major role for stress mediated by adrenocorticotrophic hormones may be excluded because, in the present study, adrenalectomy failed to significantly alter the course of CA.…”

Section: Discussionmentioning

confidence: 66%

“…Rather, we postulate that an increase observed in the absolute number of T cells in peripheral lymphoid tissues (8) suggests active emigration and dissemination of thymocytes during schistosome infection. Whether thymocyte-specific autoantibody observed in mice with Schistosoma japonicum infection (20) and in a preliminary study in our laboratory contribute to CA and thymocyte distribution has not yet been determined. In this and another study (12), TDH cells were insensitive to adult thymectomy, suggesting that they are derived from a pool of precursor T cells present in peripheral lymphoid tissues.…”

Section: Discussionmentioning

confidence: 90%

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Atrophy of the thymic cortex in mice with granulomatous schistosomiasis mansoni

Wellhausen¹,

Boros²

1982

Infect Immun

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Thymic histopathology and granulomatous hypersensitivity were examined in CBA/J mice infected with varying numbers of Schistosoma mansoni worms. At the acute phase (8 weeks) of infection, the thymi of infected mice showed depletion of cortical lymphocytes that resulted in loss of distinction in the corticomedullary region. The degree of cortical depletion correlated directly with the intensity of infection, as assessed by total egg burden of the liver. Adrenalectomy of heavily infected mice 5 to 6 weeks after infection did not alter the course of cortical lymphocyte depletion. Thymus mass was diminished by as much as 80% in heavily infected mice. However, the thymi of lightly infected mice which survived 20 weeks of infection did not differ in histology or total tissue mass from age-matched uninfected controls. Adult thymectomy at 3 weeks of infection did not abrogate the spontaneous modulation (diminution) of granuloma formation in 20-week infected mice, although spleen cells from these mice failed to adoptively transfer suppression. Heavily infected mice which did not survive beyond the acute phase (8 to 9 weeks) of infection displayed a diminished granulomatous response that was partially restored by thymectomy carried out at 5 to 6 weeks of infection. Spleen cells from heavily infected mice (8 weeks) adoptively suppressed the granulomatous response in lightly infected recipients. It is concluded that histological changes observed in the thymus concurrent with egg dissemination and granulomatous hypersensitivity correlated with T cell-mediated regulatory events.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 90%

Atrophy of the thymic cortex in mice with granulomatous schistosomiasis mansoni

Wellhausen¹,

Boros²

1982

Infect Immun

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“…A possibility was a numerical deficiency of one or more of the cell populations required for this response. The deficiency might be due to actual destruction of cells by autoantibodies (13) and/or to the emigration of cells from the spleen to other sites, especially to the hepatic granulomas which contain SEA (28). The cell populations required for the induction of cellular immune responses in general and granulomatous inflammation in particular include antigen-presenting cells (APC) such as macrophages and B cells expressing major histocompatibility complex surface class II molecules and L3T4+ T cells which actually produce the IL-2 and are required for the expression of granulomatous inflammation (18).…”

Section: Resultsmentioning

confidence: 99%

Deficiency of interleukin-2 activity upon addition of soluble egg antigen to cultures of spleen cells from mice infected with Schistosoma japonicum

Stavitsky

Harold

1988

Infect Immun

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Schistosomajaponicum-infected C57BL/6 mice show similar dynamics of hepatic granulomatous inflammation (HGI) and delayed hypersensitivity (DH) elicited by soluble egg antigens (SEA) which reach peak levels at 9 weeks of infection and then spontaneously regress. The in vitro SEA-induced proliferation of spleen cells (SC) from infected animals attained its high point and then declined when SC from 5-week-infected mice were used. The present study determined the dynamics of interleukin-2 (IL-2) production by SEA-challenged SC from infected mice in an attempt to link the level of IL-2 production to the spontaneous regression of the aforementioned T-cell-mediated immune responses. The production of IL-2 by SEA-stimulated SC reached its peak when cells from 7-week-infected mice were challenged at least 2 weeks after the peak of the proliferative response, but declined at about the same time as the HGI and DH responses. Therefore, the decline in IL-2 activity cannot alone explain the diminished proliferative response but could account for the reduction in HGI and DH in vivo. Some possible mechanisms that might explain the IL-2 deficiency were examined. This deficiency is not due to the in vitro binding of IL-2 by the SC of infected mice and is, therefore, likely to be due to underproduction of IL-2. Nor is the deficiency explained by reduced numbers of antigen-presenting cells (macrophages and B cells) or of L3T4+ T lymphocytes or by suppression of IL-2 production by macrophages or macrophage products such as prostaglandins. However, suppression of IL-2 production was observed consistently upon coculture of SC from acutely infected mice with SC from mice infected for 10 weeks. The cells which suppress appear to be Lyt2+ T cells. The data are consistent with the hypothesis that suppressor T cells inhibit the production of IL-2 and perhaps of other cytokines or Iymphokines and that this suppression explains the spontaneous down-regulation of HGI which occurs during schistosomiasis japonica.

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“…21,22 Already in the 1980s, relatively high levels of auto-reactive antibodies were reported in connection with chronic schistosomiasis. 23,24 The connection between longliving helminth parasites and the development of such antibodies have recently become increasingly observed and commented on, in particular with respect to schistosomes. [25][26][27] This study was conducted to find out whether patients with S. japonicum infection are at a particular risk of autoimmune disease.…”

Section: Introductionmentioning

confidence: 99%

“…However, this response pattern can “backfire” and trigger auto‐immunological reactions . Already in the 1980s, relatively high levels of auto‐reactive antibodies were reported in connection with chronic schistosomiasis . The connection between long‐living helminth parasites and the development of such antibodies have recently become increasingly observed and commented on, in particular with respect to schistosomes …”

Section: Introductionmentioning

confidence: 99%

Antinuclear antibodies and interleukin responses in patients with Schistosoma japonicum infection

Wang

Song

et al. 2018

Parasite Immunology

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Schistosomiasis poses a serious threat to public health, and the infection will develop into chronic and advanced late-stage disease if not treated. Apart from the clinical signs due to immune reactions to schistosome eggs trapped in host tissues, it also increases the risk for the development of autoimmunity reflected by dysfunctional, auto-reactive antibodies. Antinuclear antibodies (ANA) have been reported in schistosomiasis due to S. mansoni and S. haematobium. We demonstrate ANA in schistosomiasis japonica and explore the relationship between this infection and autoimmune disease by measuring ANA and interleukin (IL)-10, IL-12 and IL-17 responses in the sera of 125 Chinese patients with different stages of schistosomiasis japonica. The incidence rates of ANA in the patients with acute, chronic and late stages of schistosomiasis infection were 6.7%, 23.3% and 70.0%, respectively, with statistically significant differences between each stage (P = 0.000). IL-17 concentrations were high at the acute stage of schistosomiasis compared to the other stages of the disease (P = 0.000). This pattern was also seen for IL-10 and IL-12 concentrations (P = 0.01). IL concentrations in patients in the chronic and late stages of the disease were low and showed no difference compared to the healthy adults.

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Thymocytotoxic autoantibodies found in mice infected with Schistosoma japonicum

Cited by 13 publications

References 10 publications

Atrophy of the thymic cortex in mice with granulomatous schistosomiasis mansoni

Atrophy of the thymic cortex in mice with granulomatous schistosomiasis mansoni

Deficiency of interleukin-2 activity upon addition of soluble egg antigen to cultures of spleen cells from mice infected with Schistosoma japonicum

Antinuclear antibodies and interleukin responses in patients with Schistosoma japonicum infection

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