Role of murine intestinal intraepithelial lymphocytes and lamina propria lymphocytes against primary and challenge infections with Cryptosporidium parvum

Sang Mee Guk, Tai Soon Yong, Jong Yil Chai

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

To investigate the role of intestinal lamina propria lymphocytes (LPL) and intraepithelial lymphocytes (IEL) in controlling Cryptosporidium parvum infection, changes in their phenotypes and functional properties were studied after induction of primary and challenge infections in immunocompetent mice. As shown by oocyst-shedding patterns, the challenge-infected group recovered more rapidly from infection than did the primary-infected group. In LPL, proportions of activated CD4+, CD25+, IgG1+, IgA+, and CD4+/IFN-γ+ cells increased significantly in the primary-infected group compared with controls. In the challenge-infected group, proportions of these cells decreased. The antigen-specific IgA level was elevated significantly among LPL of both primary- and challenge-infected groups. Among IEL, proportions of activated CD8+, T cell receptor (TCR) γδ+, and CD8+/TCR γδ+ cells increased significantly in the challenge-infected group compared with controls and the primary-infected group; their cytotoxicity also was enhanced. However, the proportion of IEL expressing Th1 cytokines was lower than that among LPL in both infected groups. The results suggest that LPL play a more important role in protection against a primary infection with C. parvum, through the production of IFN-γ and IgA, whereas IEL are more involved in protection against a challenge infection, through enhanced cytotoxicity.

Original languageEnglish
Pages (from-to)270-275
Number of pages6
JournalJournal of Parasitology
Volume89
Issue number2
DOIs
Publication statusPublished - 2003 Apr 1

Fingerprint

Cryptosporidium parvum
Mucous Membrane
lymphocytes
Lymphocytes
mice
Infection
infection
Immunoglobulin A
T-Cell Antigen Receptor
antigen
cytotoxicity
phenotype
T-lymphocytes
receptors
Oocysts
cells
oocysts
functional properties
cytokines
Immunoglobulin G

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Ecology, Evolution, Behavior and Systematics

Cite this

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title = "Role of murine intestinal intraepithelial lymphocytes and lamina propria lymphocytes against primary and challenge infections with Cryptosporidium parvum",
abstract = "To investigate the role of intestinal lamina propria lymphocytes (LPL) and intraepithelial lymphocytes (IEL) in controlling Cryptosporidium parvum infection, changes in their phenotypes and functional properties were studied after induction of primary and challenge infections in immunocompetent mice. As shown by oocyst-shedding patterns, the challenge-infected group recovered more rapidly from infection than did the primary-infected group. In LPL, proportions of activated CD4+, CD25+, IgG1+, IgA+, and CD4+/IFN-γ+ cells increased significantly in the primary-infected group compared with controls. In the challenge-infected group, proportions of these cells decreased. The antigen-specific IgA level was elevated significantly among LPL of both primary- and challenge-infected groups. Among IEL, proportions of activated CD8+, T cell receptor (TCR) γδ+, and CD8+/TCR γδ+ cells increased significantly in the challenge-infected group compared with controls and the primary-infected group; their cytotoxicity also was enhanced. However, the proportion of IEL expressing Th1 cytokines was lower than that among LPL in both infected groups. The results suggest that LPL play a more important role in protection against a primary infection with C. parvum, through the production of IFN-γ and IgA, whereas IEL are more involved in protection against a challenge infection, through enhanced cytotoxicity.",
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Role of murine intestinal intraepithelial lymphocytes and lamina propria lymphocytes against primary and challenge infections with Cryptosporidium parvum. / Guk, Sang Mee; Yong, Tai Soon; Chai, Jong Yil.

In: Journal of Parasitology, Vol. 89, No. 2, 01.04.2003, p. 270-275.

Research output: Contribution to journalArticle

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