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Proc Natl Acad Sci U S A. 2015 Jun 30;112(26):E3412-20. doi: 10.1073/pnas.1420078112. Epub 2015 Jun 15.

Hemocyte differentiation mediates the mosquito late-phase immune response against Plasmodium in Anopheles gambiae.

Author information

1
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205;
2
Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852.
3
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205; mlorena@jhsph.edu.

Abstract

Plasmodium parasites must complete development in the mosquito vector for transmission to occur. The mosquito innate immune response is remarkably efficient in limiting parasite numbers. Previous work has identified a LPS-induced TNFα transcription factor (LITAF)-like transcription factor, LITAF-like 3 (LL3), which significantly influences parasite numbers. Here, we demonstrate that LL3 does not influence invasion of the mosquito midgut epithelium or ookinete-to-oocyst differentiation but mediates a late-phase immune response that decreases oocyst survival. LL3 expression in the midgut and hemocytes is activated by ookinete midgut invasion and is independent of the mosquito microbiota, suggesting that LL3 may be a component of a wound-healing response. LL3 silencing abrogates the ability of mosquito hemocytes to differentiate and respond to parasite infection, implicating hemocytes as critical modulators of the late-phase immune response.

KEYWORDS:

hemocytes; innate immune response; late-phase immunity; malaria; mosquito

PMID:
26080400
PMCID:
PMC4491748
DOI:
10.1073/pnas.1420078112
[Indexed for MEDLINE]
Free PMC Article

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