Characteristics of invasive candidiasis in IFN-$gamma; and IL-4 deficient mice: The role of macrophages in host defense against C. Albicans

Káposzta, Rita

doi:10.1016/s0161-5890(98)90464-3

Cited by 39 publications

(54 citation statements)

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“…ConA is also known to induce anti-fungal response (Felipe et al 1995). This effect seems to be mediated by IFN-γ production through development of Th1 cells, leading to the activation of phagocytes (Kaposzta et al 1998). Based on our finding, HVEM might be also implicated in these immune responses and is a potential target for their modulation.…”

Section: Discussionsupporting

confidence: 51%

Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule

Ando

Yasuoka

Mishima

et al. 2013

In Vitro Cell.Dev.Biol.-Animal

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T cell activation is regulated by two distinct signals, signal one and two. Concanavalin A (ConA) is an antigen-independent mitogen and functions as signal one inducer, leading T cells to polyclonal proliferation. CD28 is known to be one of major costimulatory receptors and to provide signal two in the ConA-induced T cell proliferation. Here, we have studied the implication of other costimulatory pathways in the ConA-mediated T cell proliferation by using soluble recombinant proteins consisting of an extracellular domain of costimulatory receptors and Fc portion of human IgG. We found that T cell proliferation induced by ConA, but not PMA plus ionomycin or anti-CD3 mAb, is significantly inhibited by HVEM-Ig, even in the presence of CD28 signaling. Moreover, the high concentration of HVEM-Ig molecules almost completely suppressed ConA-mediated T cell proliferation. These results suggest that HVEM might play more important roles than CD28 in ConA-mediated T cell proliferation.

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Section: Discussionsupporting

confidence: 51%

Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule

Ando

Yasuoka

Mishima

et al. 2013

In Vitro Cell.Dev.Biol.-Animal

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“…While the monoclonal 7/4 antibody defines a polymorphic neutrophil differentiation antigen (Hirsch and Gordon, 1983), more recently it has been shown to also weakly recognize immune activated macrophages (Kaposzta et al, 1998) and monocytes although the 7/4 antigen expression is reduced after exposure to LPS (Taylor et al, 2003). This emergence of this double positive 7/4 + /CD4 + population in β 2 -adrenergic receptor knock out female mice may represent a further regulation of cell surface marker by β 2 -adrenergic receptor in a subpopulation of myeloid cells Most actions of catecholamines on immune cells are believed to be mediated via β 2 - (Barnes, 1999), α 1 -(during chronic inflammation (Roupe van der Voort et al, 2000)), and α 2 -adrenergic receptors (Straub et al, 2000a).…”

Section: Discussionmentioning

confidence: 99%

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Coupade¹,

Brown²,

Dazin

et al. 2007

Journal of Neuroimmunology

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In wild-type FVB mice, leukocyte recruitment to lipopolysaccharide was sexually dimorphic, with a greater number of leukocytes recruited in females. In male β 2 -adrenergic receptor knock out mice (bred on a congenic FVB background) the number leukocytes recruited was increased ~4-fold, while in females there was no change, eliminating sexual dimorphism in leukocyte migration. While there were significantly fewer recruited CD62L + and CD11a + leukocytes in wild-type males, only in male β 2 -adrenergic receptor knock out mice was there an increase in the number of recruited CD11a + leukocytes, again eliminating sexual dimorphism. Thus, leukocyte migration and CD11a + adhesion molecule expression in male, but not in female, leukocytes is β 2 -adrenergic receptor-dependent. Our findings provide support for a role of β 2 -adrenergic receptor mechanisms in the inflammatory response, and suggest that β 2 -adrenergic receptor on male leukocytes contributes to sexual dimorphism in the effect of stress on inflammatory diseases.

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“…1,25(OH) 2 D 3 has some paradoxical effects on host resistance to infections. Even though IFN-γ production is critical for survival from Candida albicans infection; 1,25(OH) 2 D 3 treatment of mice had no effect on survival from systemic candidiasis Kaposzta et al 1998). For TB there is anecdotal evidence that perhaps vitamin D deficiency and reduced sunlight exposure result in more severe TB (Gibney et al 2008).…”

Section: Vitamin D and Th1 Mediated Host Immunity To Infectionmentioning

confidence: 99%

“…Th1 mediated immunity is critical for the ability of the host to mount a protective immune response to many different infections. Paradoxically, 1,25(OH) 2 D 3 treatments did not compromise the ability of infected mice to fight a fungal infection that depends on Th1 mediated immunity Kaposzta et al 1998). Furthermore, vitamin D status and 1,25 (OH) 2 D 3 have been suggested to be protective against tuberculosis (TB) where host immunity depends on Th1 production of the cytokine IFN-γ.…”

Section: Introductionmentioning

confidence: 99%

The paradoxical effects of vitamin D on type 1 mediated immunity

Cantorna

Bruce

2008

Molecular Aspects of Medicine

120

115

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Low vitamin D status is associated with an increased risk of Th1 mediated autoimmune diseases like inflammatory bowel disease. 1,25(OH) 2 D 3 treatments have been shown to suppress Th1 mediated immunity and protect animals from experimental autoimmunity. Th1 mediated immunity is important for clearance of a number of different infectious diseases. For tuberculosis 1,25(OH) 2 D 3 treatment is associated with decreased Th1 mediated immunity but increased bactericidal activity. Systemic candidiasis is unaffected by 1,25(OH) 2 D 3 treatment. The seemingly paradoxical effects of 1,25(OH) 2 D 3 and vitamin D on Th1 mediated autoimmunity versus infectious immunity point to a broad array of vitamin D targets in the immune system. The interplay of these vitamin D targets and their impact on the host-immune response then dictate the outcome.

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Characteristics of invasive candidiasis in IFN-$gamma; and IL-4 deficient mice: The role of macrophages in host defense against C. Albicans

Cited by 39 publications

References 0 publications

Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule

Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

The paradoxical effects of vitamin D on type 1 mediated immunity

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