Resistance of Mice Deficient in IL-4 to Retrovirus-Induced Immunodeficiency Syndrome (MAIDS)

Kanagawa, Osami; Vaupel, Barbara A.; Gayama, Shinyo; Koehler, Georges; Köpf, Manfred

doi:10.1126/science.8211142

Cited by 101 publications

(33 citation statements)

References 21 publications

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“…Clerici et al (12,13) suggested that, during the early stages of HIV-1 infection, there is a switch from "T H 1-like" toward a "T H 2-like" pattern of cytokine production. This hypothesis was indirectly supported by the observation that IL-4 gene-targeted mice lacking T H 2 responses do not develop murine AIDS (14). However, the association with another gene product is a prerequisite for nondevelopment of murine AIDS (15).…”

Section: Hiv-1 Gp120 Induces Il-4 and Il-13 Release From Humansupporting

confidence: 50%

HIV-1 gp120 Induces IL-4 and IL-13 Release from Human FcεRI+ Cells Through Interaction with the VH3 Region of IgE

Florio

Petraroli

Marone

2000

The Journal of Immunology

140

135

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HIV-1 glycoprotein (gp) 120 from different clades is a potent stimulus for IL-4 and IL-13 release from basophils purified from healthy individuals seronegative for Abs to HIV-1 and HIV-2. IL-4 mRNA, constitutively present in basophils, was increased after stimulation by gp120 and was inhibited cyclosporin A and tacrolimus. IL-4 and IL-13 secretion from basophils activated by gp120 was not correlated. There was a correlation between the maximum gp120- and anti-IgE-induced IL-4 release from basophils. The average t1/2 gp120-induced IL-4 release was lower than for IL-13 release. Basophils from which IgE had been dissociated by brief exposure to lactic acid no longer released IL-4 in response to gp120 or to anti-IgE. The response to a mAb cross-linking the α-chain of high-affinity receptor for IgE (FcεRI) was unaffected by this treatment. Three human VH3+ monoclonal IgM inhibited gp120-induced secretion of IL-4 from basophils. In contrast, VH6+ monoclonal IgM did not inhibit the release of IL-4 induced by gp120. Synthetic peptides distant from the NH2 and COOH termini of gp120MN inhibited the activating property of gp120MN. These results indicate that gp120, which acts as a viral superantigen, interacts with the VH3 region of IgE to induce the release of IL-4 and IL-13 from human FcεRI+ cells.

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Section: Hiv-1 Gp120 Induces Il-4 and Il-13 Release From Humansupporting

confidence: 50%

HIV-1 gp120 Induces IL-4 and IL-13 Release from Human FcεRI+ Cells Through Interaction with the VH3 Region of IgE

Florio

Petraroli

Marone

2000

The Journal of Immunology

140

135

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“…The acute host response to a primary HIV infection is characterized by a Th0 cytokine profile including the proinflammatory cytokines IL-1, IL-2, IL-6, TNF-␣, IFN-␣/␤, and IFN-␥ (86,202,238), as well as the anti-inflammatory cytokines IL-4, IL-10, and IL-13 (86,190). At later stages of infection, as full-blown AIDS progresses, the pattern of cytokine production shifts toward a strongly biased Th2-like response (47,48,115). The mechanisms of HIV-induced cytokine production have been studied in great detail, and much information is available about the early cytokine expression whereas less is known about what causes the shift in cytokine profile.…”

Section: Human Immunodeficiency Virusmentioning

confidence: 99%

Molecular Pathways in Virus-Induced Cytokine Production

Mogensen

Paludan

2001

Microbiol Mol Biol Rev

358

324

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Virus infections induce a proinflammatory response including expression of cytokines and chemokines. The subsequent leukocyte recruitment and antiviral effector functions contribute to the first line of defense against viruses. The molecular virus-cell interactions initiating these events have been studied intensively, and it appears that viral surface glycoproteins, double-stranded RNA, and intracellular viral proteins all have the capacity to activate signal transduction pathways leading to the expression of cytokines and chemokines. The signaling pathways activated by viral infections include the major proinflammatory pathways, with the transcription factor NF-κB having received special attention. These transcription factors in turn promote the expression of specific inducible host proteins and participate in the expression of some viral genes. Here we review the current knowledge of virus-induced signal transduction by seven human pathogenic viruses and the most widely used experimental models for viral infections. The molecular mechanisms of virus-induced expression of cytokines and chemokines is also analyzed

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“…In contrast to Th1 cells, Th2 cells secrete IL-4 and stimulate B-cell proliferation and differentiation to produce predominantly IgG1 and IgE antibodies (39). The balance between Th1 and Th2 cells plays a major role in immunity and pathogenesis for several infectious diseases (10), including possible roles in infections by human immunodeficiency virus (9,61) and murine AIDS virus (19,33,45). However, little is known about the role of cytokines in primary immune responses and vaccinemediated protection against retroviral infections.…”

mentioning

confidence: 99%

Role of Interleukin-4 (IL-4), IL-12, and Gamma Interferon in Primary and Vaccine-Primed Immune Responses to Friend Retrovirus Infection

Dittmer

Peterson

Messer

et al. 2001

J Virol

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The immunological resistance of a host to viral infections may be strongly influenced by cytokines such as interleukin-12 (IL-12) and gamma interferon (IFN-␥), which promote T helper type 1 responses, and IL-4, which promotes T helper type 2 responses. We studied the role of these cytokines during primary and secondary immune responses against Friend retrovirus infections in mice. IL-4-and IL-12-deficient mice were comparable to wild-type B6 mice in the ability to control acute and persistent Friend virus infections. In contrast, more than one-third of the IFN-␥-deficient mice were unable to maintain long-term control of Friend virus and developed gross splenomegaly with high virus loads. Immunization with a live attenuated vaccine virus prior to challenge protected all three types of cytokine-deficient mice from viremia and high levels of spleen virus despite the finding that the vaccinated IFN-␥-deficient mice were unable to class switch from immunoglobulin M (IgM) to IgG virus-neutralizing antibodies. The results indicate that IFN-␥ plays an important role during primary immune responses against Friend virus but is dispensable during vaccine-primed secondary responses.

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Resistance of Mice Deficient in IL-4 to Retrovirus-Induced Immunodeficiency Syndrome (MAIDS)

Cited by 101 publications

References 21 publications

HIV-1 gp120 Induces IL-4 and IL-13 Release from Human FcεRI+ Cells Through Interaction with the VH3 Region of IgE

HIV-1 gp120 Induces IL-4 and IL-13 Release from Human FcεRI+ Cells Through Interaction with the VH3 Region of IgE

Molecular Pathways in Virus-Induced Cytokine Production

Role of Interleukin-4 (IL-4), IL-12, and Gamma Interferon in Primary and Vaccine-Primed Immune Responses to Friend Retrovirus Infection

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