Cellular Immunity to Herpes Simplex Virus Mediated by Interferon

Lodmell, Donald L.; Notkins, Abner Louis

doi:10.1084/jem.140.3.764

Cited by 58 publications

(20 citation statements)

References 23 publications

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“…

Recent studies have revealed that peripheral T cells express different Lytalloantigens on their surfaces and are divisible into three subpopulations with phenotypes Lyt-1.2.3, Lyt-l, and Lyt-2.3 (2).

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mentioning

confidence: 99%

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Role of Lyt‐1 Positive Immune T Cells in Recovery from Herpes Simplex Virus Infection in Mice

Nagafuchi

Hayashida

Higa

et al. 1982

Microbiology and Immunology

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It has been shown that T cell-mediated immunity plays a major role (4,5,(7)(8)(9)(10)12) in control of and recovery from herpes simplex virus (HSV) infection. Nevertheless, the mechanism of immune T cell-mediated protection in vivo is complex and poorly understood.Recent studies have revealed that peripheral T cells express different Lytalloantigens on their surfaces and are divisible into three subpopulations with phenotypes Lyt-1.2.3, Lyt-l, and Lyt-2.3 (2). Lyt-1.2.3 cells are presumed to be precursors for Lyt-I or Lyt-2.3 cells (2). Lyt-l cells are programmed to help or amplify activities of other cells after stimulation by an antigen (2). They help B cells to produce antibody and activate macrophages in the generation of the delayed type hypersensitivity reaction (2). Lyt-2.3 cells are known to suppress antibody production and other immune responses, and to be cytotoxic cells (2).In this study, we have used Lyt-alloantisera for the examination of immune T lymphocytes responsible for providing protection in mice lethally infected with HSV.Six-to 10-week-old athymic nude (nu/nu) mice and their littermates (nu/+) with BALB/c genetic background were purchased from the Central Laboratories of Experimental Animals Co., Ltd., Japan. When athymic nude mice were injected intracutaneously with 2.5 X 10 4 plaque-forming units (PFU) of the virulent Hayashida strain of HSV-l per 0.05 ml, all of the mice died after development of severe zosteriform skin lesions, while all of the control nul + mice survived the infection, as reported previously (10), indicating that resistance of HSV infection is T-cell dependent.In order to determine the phenotypes of committed lymphocytes responsible for HSV resistance, immune spleen cells were transferred to numu mice that were lethally infected with HSV, following treatment with various antilymphocyte sera. Anti-lymphocyte alloantisera were obtained from Cederlane Laboratories, Canada. Anti-Thy-1.2 alloantisera were produced in AKR/J mice by injecting thymocytes

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“…

Recent studies have revealed that peripheral T cells express different Lytalloantigens on their surfaces and are divisible into three subpopulations with phenotypes Lyt-1.2.3, Lyt-l, and Lyt-2.3 (2).

…”

mentioning

confidence: 99%

“…It has been shown that T cell-mediated immunity plays a major role (4,5,(7)(8)(9)(10)12) in control of and recovery from herpes simplex virus (HSV) infection. Nevertheless, the mechanism of immune T cell-mediated protection in vivo is complex and poorly understood.…”

mentioning

confidence: 99%

Role of Lyt‐1 Positive Immune T Cells in Recovery from Herpes Simplex Virus Infection in Mice

Nagafuchi

Hayashida

Higa

et al. 1982

Microbiology and Immunology

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“…Thus, not only could viral replication be triggered or be enhanced by cyclic nucleotide changes, but also the antiviral, activity of IFN on HSV could be suppressed. The spread of the herpesviruses to contiguous uninfected cells, which has been shown to be influenced by IFN (14), might then be affected.…”

Section: Discussionmentioning

confidence: 98%

Effect of cyclic AMP and cyclic GMP on the activity of interferon against herpes simplex virus types 1 and 2, and vesicular stomatitis virus

Stanwick

Nahmias

1982

Archives of Virology

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The antiviral action of interferon (IFN) on herpes simplex virus (HSV) types 1 and 2, and vesicular stomatitis virus (VSV) was examined with respect to the intracellular levels of cyclic adenosine monophosphate (CAMP) and cyclic guanosine monophosphate (CGMP) in human fibroblast (HF) cultures. Interferon by itself increased the intracellular levels of CAMP, but had no effect on the CGMP levels. Inoculation of HF with HSV, however, decreased the CAMP levels. Also, HSV inoculation elevated the CGMP levels, but VSV did not alter the CGMP levels. When HSV and IFN were added to the HF cultures in various combinations, HSV inhibited the IFN-induced elevation of CAMP and increased the CGMP levels to that characteristically observed with HSV inoculation in the absence of IFN. In contrast, IFN antagonized the VSV-associated decrease in CAMP levels. Although the yields of VSV were unaltered by the presence of CAMP- or CGMP-enhancing compounds, the yields of HSV were decreased with CAMP enhancers and increased with CGMP enhancers. the combination of IFN and CAMP enhancers had an additive effect in reducing the yields of HSV. Neither the CAMP or CGMP enhancers affected the action of IFN on VSV. These studies suggest that the interactions observed between HSV and cyclic nucleotides might account for the relatively refractive nature of HSV, as compared to VSV, toward the antiviral activity of IFN.

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“…Interferon was shown by Lodmell and Notkins [73] to be produced by rabbit leukocytes sensitized to PPD and stimulated with PPD or by leukocytes sensitized and then stimulated by HSV. Peritoneal exudate cells were more effective than spleen cells in each case, suggesting that macrophages were important in the response.…”

Section: Lymphocyte Interferon Productionmentioning

confidence: 97%