Exogenous interleukin-2 abrogates differences in the proliferative responses to T cell mitogens among inbred strains of mice

Lipoldová, Marie; Zajı́cová, Alena; Stĕdra, J; Holáň, Vladimı́r

doi:10.1016/0008-8749(92)90278-w

Cited by 10 publications

(10 citation statements)

References 28 publications

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“…The gelatinase group of MMPs, which includes MMP-2 and MMP-9, cleave soluble fragments of collagen and promote the development of infarct rupture [31]. Moreover, CD4 + T cells from C57BL/6 mice produce lower levels of IL-2 than BALB/c mice [34,35]. However, cardiac rupture did not occur until later than 3 days in that study.…”

Section: Discussionmentioning

confidence: 61%

Enhanced monocyte recruitment and delayed alternative macrophage polarization accompanies impaired repair following myocardial infarction in C57BL/6 compared to BALB/c mice

Toor

Rückerl

Mair

et al. 2019

Clinical and Experimental Immunology

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Summary Activation of the innate immune response following myocardial infarction (MI) is essential for infarct repair. Preclinical models of MI commonly use C57BL/6 mice, which have a type 1‐dominant immune response, whereas other mouse strains such as BALB/c mice have a type 2‐dominant immune response. We compared C57BL/6 and BALB/c mice to investigate whether predisposition towards a proinflammatory phenotype influences the dynamics of the innate immune response to MI and associated infarct healing and the risk of cardiac rupture. MI was induced by permanent coronary artery ligation in 12–15‐week‐old male wild‐type BALB/c and C57BL/6 mice. Prior to MI, C57BL/6 mice had a lower proportion of CD206+ anti‐inflammatory macrophages in the heart and an expanded blood pool of proinflammatory Ly6Chigh monocytes in comparison to BALB/c mice. The systemic inflammatory response in C57BL/6 mice following MI was more pronounced, with greater peripheral blood Ly6Chigh monocytosis, splenic Ly6Chigh monocyte mobilization and myeloid cell infiltration of pericardial adipose tissue. This led to an increased and prolonged macrophage accumulation, as well as delayed transition towards anti‐inflammatory macrophage polarization in the infarct zone and surrounding tissues of C57BL/6 mice. These findings accompanied a higher rate of mortality due to cardiac rupture in C57BL/6 mice compared with BALB/c mice. We conclude that lower post‐MI survival of C57BL/6 mice over BALB/c mice is mediated in part by a more pronounced and prolonged inflammatory response. Outcomes in BALB/c mice highlight the therapeutic potential of modulating resolution of the innate immune response following MI for the benefit of successful infarct healing.

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Section: Discussionmentioning

confidence: 61%

Enhanced monocyte recruitment and delayed alternative macrophage polarization accompanies impaired repair following myocardial infarction in C57BL/6 compared to BALB/c mice

Toor

Rückerl

Mair

et al. 2019

Clinical and Experimental Immunology

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“…It was previously documented that IL-2 increased the limited in vitro proliferation of ConA-stimulated spleen cells of B10 mice [10]; this finding pointed to a lack of IL-2 production in the B10 cells [9,10]. Specific anti-SRBC IgG response in vitro could be restored to a certain degree by the presence of IL-2 in the culture medium [9].…”

Section: The Ag-specific In Vitro Response Cannot Be Manipulated By Il-2mentioning

confidence: 88%

“…Lipoldová et al [10] documented the retained capability of B10 cells to respond to IL-2, as ConA-stimulated B10 spleen cells highly proliferate in the presence of exogenous IL-2, whereas without IL-2 their proliferation is significantly lower when compared with BALB/c cells. This also corresponds with our finding that in vitro induced secondary antibody response in B10 mice could be stimulated by exogenous IL-2 up to the level detected in A/J cells without IL-2 [9].…”

Section: The Functional Capacity Of T Helper Cell Population Is Indismentioning

confidence: 99%

“…Constraints in antigen-presenting capacity were directly proven using in vitro antigen (SRBC)-pulsed peritoneal macrophages isolated either from B10 or A/J mice and restimulated in vivo after the transfer to (A/J 2 B10)F1 recipients [8]. Moreover, we [9] and others [10] have shown that in vitro production of interleukin-2 (IL-2) and interleukin-3 (IL-3) after a mitogenic signal delivered by the CD3-TCR complex is limited in the low responding strain B10. Thus, both the impaired antigen-presenting capacity of macrophages and suspected intrinsic T-cell defect may account for the limited IgG antibody response in the B10 strain.…”

Section: Introductionmentioning

confidence: 99%

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Limited T Helper Cell Activity in C57BL/10 (B10) Mice with Inherited Low IgG Responsiveness

1996

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Due to limitations in antigen processing, mice of the C57BL/10ScSn (B10) strain exhibit a low IgG production against a variety of T-dependent antigens. To characterize the T-cell functions, the authors studied antigen-specific T-cell proliferation and cytokine production in vitro. The response of B10 mice was compared with that of the high IgG producing strain A/J. A highly restricted proliferative response and almost no interleukin-2 (IL-2) and interleukin-3 (IL-3) production was detected in lymph node (LN) cells of B10 mice primed in vivo by protein antigens and subjected to a specific restimulation in vitro, whilst A/J cells responded by significant proliferation and cytokine production. The antigen-specific T-cell response of B10 mice could not be increased by lipopolysaccharide treatment in vivo or by in vitro cultivation with IL-2. However, the T cells of B10 mice produced high levels of IL-2 and IL-4 when stimulated by phorbol myristate acetate (PMA) and Ca2+ ionophore, proving the existence of a functionally intact signal transduction pathway downstream of protein kinase C (PKC). The results suggest that the in vivo antigen priming does not effectively activate the T cells in B10 mice. The limited activation consequently leads to the low IgG response described in B10 mice.

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“…In some experimental situations. IL-2 is sufficient to normalize Tcell proliferative responses [31,32], which was not the case in BN rats, indicating that other factors such as NO [8] are responsible for the defect. The fact that the specific cytotoxic response oi" normal BN lymphocytes was normalized in the presence oflL-2 while the MLR was increased only slightly deserves discussion.…”

Section: Discussionmentioning

confidence: 99%

Improvement of TH1 Functions during the Regulation Phase of Mercury Disease in Brown Norway Rats

et al. 1994

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Brown Norway (BN) rats are poor responders to T-cell mitogens and alloantigens when compared to Lewis (LEW) rats. This is dependent partly upon a defect in IL-2 production. The TH2-mediated immune abnormalities observed in BN rats injected with mercuric chloride (HgCl2) are self-limited and it is probable that this regulation phase involves TH1-like cells. This paper reports on a study of the ability of lymph node cells (LNC) from normal BN and LEW rats and from HgCl2-injected BN rats to produce IL-2 and to proliferate when stimulated in vitro by Con A or alloantigens in mixed lymphocyte reaction (MLR), as well as to develop a cytotoxic T lymphocyte (CTL) response to alloantigens. This study will confirm that LNC from BN rats proliferate less than LNC from LEW rats, that the former produce less IL-2 than the latter, and that the proliferative response is restored partially after addition of IL-2. In addition, it is shown (1) that the CTL response is defective in normal BN rats when compared to that of normal LEW rats, and (2) that, after the second week of HgCl2 injections, the proliferative responses to Con A and alloantigens are improved as well as IL-2 production, and a complete restoration of CTL function is observed. These results show that normal BN rats are deficient in the induction of TH1-like cells and that, from the second week of HgCl2 injections, these TH1 functions improve.

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Exogenous interleukin-2 abrogates differences in the proliferative responses to T cell mitogens among inbred strains of mice

Cited by 10 publications

References 28 publications

Enhanced monocyte recruitment and delayed alternative macrophage polarization accompanies impaired repair following myocardial infarction in C57BL/6 compared to BALB/c mice

Enhanced monocyte recruitment and delayed alternative macrophage polarization accompanies impaired repair following myocardial infarction in C57BL/6 compared to BALB/c mice

Limited T Helper Cell Activity in C57BL/10 (B10) Mice with Inherited Low IgG Responsiveness

Improvement of TH1 Functions during the Regulation Phase of Mercury Disease in Brown Norway Rats

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