Recombinant Interleukin-1?, Interleukin-2 and M-CSF-1 enhance the survival of newborn C57BL/6 mice inoculated intraperitoneally with a lethal dose of herpes simplex virus-1

Berkowitz, Cheryl; Becker, Yechiel

doi:10.1007/bf01314627

Cited by 15 publications

(5 citation statements)

References 39 publications

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“…HSV‐1 infection of gD3‐vaccinated mice resulted in a strong Th1 response, as indicated by the presence of IL‐2 and TNF‐α. 9 Similar to our results, it has been shown that, recombinant IL‐2 31 and TNF‐α32 can protect mice against lethal HSV‐1 infection and eye disease. We postulate that the reduced viral replication seen in the gD3 mice was because of a combination of this strong Th1 response (IL‐2 and TNF‐α) and high neutralizing antibody titres.…”

Section: Discussionsupporting

confidence: 88%

The role of neutralizing antibody and T‐helper subtypes in protection and pathogenesis of vaccinated mice following ocular HSV‐1 challenge

et al. 1998

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In order to determine the possible correlation of specific immune responses with protection against mortality and ocular disease following ocular herpes simplex virus type 1 (HSV-1) challenge, BALB/c mice were vaccinated with different doses and regimens of baculovirus-expressed gD. Neutralizing antibody, virus titres in the eyes, corneal scarring, and survival were measured. In addition, infiltration into the cornea of CD4+ T cells and cells containing the lymphokines interleukin-2 (IL-2), IL-4, IL-6 and tumour necrosis factor-alpha (TNF-alpha) were monitored on days 3, 7, 10, 14 and 21 post-challenge by immunocytochemistry. The vaccination regimens used induced varying degrees of immune responses and protection upon ocular challenge with HSV-1. Our results suggest that neutralizing antibody was the most important immune response in protecting mice against lethal ocular challenge and corneal scarring. TNF-alpha and IL-2 were not crucial in terms of survival and corneal scarring, since gD1 (one vaccination with 1 microg of gD) and gD0.1 (one vaccination with 0.1 microg of gD), both of which provided high levels of protection, showed no TNF-alpha or IL-2 expression. However, TNF-alpha and IL-2 were crucial in terms of virus clearance from the eyes, since gD3 (three vaccinations with 1 microg of gD), which had less virus in their eyes, had high numbers of TNF-alpha and IL-2 infiltrates. Finally, mock-vaccinated mice were not protected from death and corneal disease following HSV-1 challenge. Eyes of mock-vaccinated mice had little or no TNF-alpha or IL-2 responses and the strongest IL-4 and IL-6 responses.

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Section: Discussionsupporting

confidence: 88%

The role of neutralizing antibody and T‐helper subtypes in protection and pathogenesis of vaccinated mice following ocular HSV‐1 challenge

et al. 1998

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“…The protective aspect of IL-2 may be in inducing the expansion of a CD4 ϩ T-helper cell population which interacts with B cells to produce specific antibodies. In addition, recombinant IL-2 appears capable of protecting mice against lethal HSV-1 infection (3). Thus, KOS vaccination may protect against corneal scarring by producing a rapid local IL-2 response following ocular challenge.…”

Section: Discussionmentioning

confidence: 99%

Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1

Ghiasi

Wechsler

Kaiwar

et al. 1995

J Virol

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To correlate specific local immune responses with protection from corneal scarring, we examined immune cell infiltrates in the cornea after ocular challenge of vaccinated mice with herpes simplex virus type 1 (HSV-1). This is the first report to examine corneal infiltrates following ocular challenge of a vaccinated mouse rather than following infection of a naive mouse. Mice were vaccinated systemically with vaccines that following ocular challenge with HSV-1 resulted in (i) complete protection against corneal disease (KOS, an avirulent strain of HSV-1); (ii) partial protection, resulting in moderate corneal disease (baculovirus-expressed HSV-1 glycoprotein E [gE]); and (iii) no protection, resulting in severe corneal disease (mock vaccine). Infiltration into the cornea of CD4 ؉ T cells, CD8 ؉ T cells, macrophages, and cells containing various lymphokines was monitored on days 0, 1, 3, 7, and 10 postchallenge by immunocytochemistry of corneal sections. Prior to ocular challenge, no eye disease or corneal infiltrates were detected in any mice. KOS-vaccinated mice developed high HSV-1 neutralizing antibody titers (>1:640) in serum. After ocular challenge, they were completely protected against death, developed no corneal disease, and had no detectable virus in their tear films at any time examined. In response to the ocular challenge, these mice developed high local levels of infiltrating CD4 ؉ T cells and cells containing interleukin-2 (IL-2), IL-4, IL-6, or tumor necrosis factor alpha (TNF-␣). In contrast, only low levels of infiltrating CD8 ؉ T cells were found, and gamma interferon (IFN-␥)-containing cells were not present until day 10. gE-vaccinated mice developed neutralizing antibody titers in serum almost as high as those of the KOS-vaccinated mice (>1:320). After ocular challenge, they were also completely protected against death. However, the gE-vaccinated mice developed low levels of corneal disease and virus was detected in one-third of their eyes. Compared with KOS-vaccinated mice, the gE-vaccinated mice had a similar pattern of IFN-␥, but a delay in the appearance of CD4 ؉ T cells, CD8 ؉ T cells, and IL-4-, IL-6-, and TNF-␣-containing cells. In sharp contrast to those of the KOS-vaccinated mice, no cells containing IL-2 were detected in the eyes of gE-vaccinated mice at any time. Mock-vaccinated mice developed no detectable neutralizing antibody titer and were not protected from lethal HSV-1 challenge. They developed the highest levels of corneal disease, and virus was detected in over 60% of their eyes. The eyes of mock-vaccinated mice had no TNF-␣ response, no IL-2 response, delayed and weaker IL-4 and IL-6 responses, and the strongest CD4 ؉ response on day 10, compared with responses of KOS-vaccinated mice. In contrast to the KOS-and gE-vaccinated mice, the mock-vaccinated mice showed an earlier and stronger CD8 ؉ T-cell response and an early IFN-␥ response. The results of this study show for the first time that in vaccinated mice ocularly challenged with HSV-1, there appears to be a correlation be...

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“…Another possible reason for lack of protection in newborn mice could be due to delayed antibody responses as well as defective macrophage and T cell function. (Berkowitz & Becker, 1992;Sarmiento, 1988). Even though all the above listed differences between newborn and adult mice logically appear to be possible reasons for the lack of protection in newborn mice, we do not have at this stage any experimental evidence to pinpoint the actual reason.…”

Section: Discussionmentioning

confidence: 99%

Protection of adult but not newborn mice against lethal intracerebral challenge with Japanese encephalitis virus by adoptively transferred virus-specific cytotoxic T lymphocytes: requirement for L3T4+ T cells

Ravi

Manjunath

1996

Journal of General Virology

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Recombinant Interleukin-1?, Interleukin-2 and M-CSF-1 enhance the survival of newborn C57BL/6 mice inoculated intraperitoneally with a lethal dose of herpes simplex virus-1

Cited by 15 publications

References 39 publications

The role of neutralizing antibody and T‐helper subtypes in protection and pathogenesis of vaccinated mice following ocular HSV‐1 challenge

The role of neutralizing antibody and T‐helper subtypes in protection and pathogenesis of vaccinated mice following ocular HSV‐1 challenge

Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1

Protection of adult but not newborn mice against lethal intracerebral challenge with Japanese encephalitis virus by adoptively transferred virus-specific cytotoxic T lymphocytes: requirement for L3T4+ T cells

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