Prevention of immune dysfunction, vitamin E deficiency, and loss of Cryptosporidium resistance during murine retrovirus infection by T cell receptor peptide immunization

Bailin Liang, John J. Marchalonis, Ronald R Watson

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

C57BL/6 mice were immunized with peptide corresponding to CDR1 of human T cell receptor (TCR) Vβ8.1 and immunoglobulin lambda-chain MCG after murine retrovirus (LP-BM5) infection. Immunization with the TCR peptide largely prevented the retrovirus-induced reduction in B and T cell proliferation, tissue vitamin E, and Th1 (T helper 1) cytokine (IL-2 and IFN-τ) secretion. The TCR peptide also prevented retrovital stimulation of Th2 cytokine (IL-6 and IL-10) production and lipid peroxidation. Cryptosporidiosis was established in all retrovirus immunosuppressed mice, while non-retrovirus infected mice were refractory to parasite infection. Cryptosporidium parvum colonization of intestinal villi was significantly reduced in immunosuppressed animals that received TCR Vβ8.1 peptide immunization. Thus, immune dysfunction with the loss of parasite resistance, induced by murine retrovirus infection, was largely prevented by TCR Vβ CDR1 peptide immunization. However, no significant change in survival of the retrovirally infected mice was observed as the lymph nodes continued to expand which induced eventual death from asphyxiation.

Original languageEnglish (US)
Pages (from-to)677-692
Number of pages16
JournalNutrition Research
Volume17
Issue number4
DOIs
StatePublished - Apr 1997

Fingerprint

Retroviridae Infections
Vitamin E Deficiency
Cryptosporidium
T-Cell Antigen Receptor
Immunization
Retroviridae
Peptides
Immunoglobulin lambda-Chains
Cytokines
Cryptosporidium parvum
Cryptosporidiosis
Parasitic Diseases
Asphyxia
Vitamin E
Inbred C57BL Mouse
Interleukin-10
Lipid Peroxidation
Interleukin-2
Interleukin-6
Parasites

Keywords

  • Cryptosporidium parvum
  • Cytokine
  • Immune Dysfunction
  • Mitogenesis
  • Murine Retrovirus Infection
  • NK Cell Activity

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Prevention of immune dysfunction, vitamin E deficiency, and loss of Cryptosporidium resistance during murine retrovirus infection by T cell receptor peptide immunization",
abstract = "C57BL/6 mice were immunized with peptide corresponding to CDR1 of human T cell receptor (TCR) Vβ8.1 and immunoglobulin lambda-chain MCG after murine retrovirus (LP-BM5) infection. Immunization with the TCR peptide largely prevented the retrovirus-induced reduction in B and T cell proliferation, tissue vitamin E, and Th1 (T helper 1) cytokine (IL-2 and IFN-τ) secretion. The TCR peptide also prevented retrovital stimulation of Th2 cytokine (IL-6 and IL-10) production and lipid peroxidation. Cryptosporidiosis was established in all retrovirus immunosuppressed mice, while non-retrovirus infected mice were refractory to parasite infection. Cryptosporidium parvum colonization of intestinal villi was significantly reduced in immunosuppressed animals that received TCR Vβ8.1 peptide immunization. Thus, immune dysfunction with the loss of parasite resistance, induced by murine retrovirus infection, was largely prevented by TCR Vβ CDR1 peptide immunization. However, no significant change in survival of the retrovirally infected mice was observed as the lymph nodes continued to expand which induced eventual death from asphyxiation.",
keywords = "Cryptosporidium parvum, Cytokine, Immune Dysfunction, Mitogenesis, Murine Retrovirus Infection, NK Cell Activity",
author = "Bailin Liang and Marchalonis, {John J.} and Watson, {Ronald R}",
year = "1997",
month = "4",
doi = "10.1016/S0271-5317(97)00037-7",
language = "English (US)",
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pages = "677--692",
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T1 - Prevention of immune dysfunction, vitamin E deficiency, and loss of Cryptosporidium resistance during murine retrovirus infection by T cell receptor peptide immunization

AU - Liang, Bailin

AU - Marchalonis, John J.

AU - Watson, Ronald R

PY - 1997/4

Y1 - 1997/4

N2 - C57BL/6 mice were immunized with peptide corresponding to CDR1 of human T cell receptor (TCR) Vβ8.1 and immunoglobulin lambda-chain MCG after murine retrovirus (LP-BM5) infection. Immunization with the TCR peptide largely prevented the retrovirus-induced reduction in B and T cell proliferation, tissue vitamin E, and Th1 (T helper 1) cytokine (IL-2 and IFN-τ) secretion. The TCR peptide also prevented retrovital stimulation of Th2 cytokine (IL-6 and IL-10) production and lipid peroxidation. Cryptosporidiosis was established in all retrovirus immunosuppressed mice, while non-retrovirus infected mice were refractory to parasite infection. Cryptosporidium parvum colonization of intestinal villi was significantly reduced in immunosuppressed animals that received TCR Vβ8.1 peptide immunization. Thus, immune dysfunction with the loss of parasite resistance, induced by murine retrovirus infection, was largely prevented by TCR Vβ CDR1 peptide immunization. However, no significant change in survival of the retrovirally infected mice was observed as the lymph nodes continued to expand which induced eventual death from asphyxiation.

AB - C57BL/6 mice were immunized with peptide corresponding to CDR1 of human T cell receptor (TCR) Vβ8.1 and immunoglobulin lambda-chain MCG after murine retrovirus (LP-BM5) infection. Immunization with the TCR peptide largely prevented the retrovirus-induced reduction in B and T cell proliferation, tissue vitamin E, and Th1 (T helper 1) cytokine (IL-2 and IFN-τ) secretion. The TCR peptide also prevented retrovital stimulation of Th2 cytokine (IL-6 and IL-10) production and lipid peroxidation. Cryptosporidiosis was established in all retrovirus immunosuppressed mice, while non-retrovirus infected mice were refractory to parasite infection. Cryptosporidium parvum colonization of intestinal villi was significantly reduced in immunosuppressed animals that received TCR Vβ8.1 peptide immunization. Thus, immune dysfunction with the loss of parasite resistance, induced by murine retrovirus infection, was largely prevented by TCR Vβ CDR1 peptide immunization. However, no significant change in survival of the retrovirally infected mice was observed as the lymph nodes continued to expand which induced eventual death from asphyxiation.

KW - Cryptosporidium parvum

KW - Cytokine

KW - Immune Dysfunction

KW - Mitogenesis

KW - Murine Retrovirus Infection

KW - NK Cell Activity

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