Title
At homeostasis filarial infections have expanded adaptive T regulatory but not classical Th2 cells
Date Issued
01 May 2010
Access level
open access
Resource Type
journal article
Author(s)
Metenou S.
Dembele B.
Konate S.
Dolo H.
Coulibaly S.Y.
Coulibaly Y.I.
Diallo A.A.
Soumaoro L.
Coulibaly M.E.
Sanogo D.
Doumbia S.S.
Traoré S.F.
Klion A.
Nutman T.B.
National Institute of Allergy and Infectious Diseases
Publisher(s)
American Association of Immunologists
Abstract
Despite the well-documented immune suppression associated with human helminth infections, studies characterizing the immune response at the single-cell level are scanty. We used multiparameter flow cytometry to characterize the type of effector (Th1, Th2, and Th17) and regulatory (natural T regulatory cells [nTregs] and adaptive Treg cells [aTreg/type 1 regulatory cells (Tr1s)]) CD4+ and CD8+ T cells in filaria-infected (Fil+) and -uninfected (Fil-) individuals at homeostasis (in the absence of stimulation). Frequencies of CD4+ lymphocytes spontaneously producing IL-4, IL-10, and IL-17A were significantly higher in Fil+, as were those of IL-10+/IL-4+ double-producing CD4+ cells. Interestingly, frequencies of Th17 and aTreg/Tr1s but not classical Th1 or Th2 cells were significantly increased in Fil+ compared to Fil- individuals. Although the frequency of nTreg was increased in Fil+, IL-10 was overwhelmingly produced by CD4+CD25- cells. Moreover, the concentration of IL-10 produced spontaneously in vitro strongly correlated with the integrated geometric mean fluorescence intensity of IL-10-producing aTreg/Tr1s in Fil +. Together, these data show that at steady state, IL-10-producing aTreg/Tr1 as well as nTreg and effector Th17 CD4+ cells are expanded in vivo in human filarial infections. Moreover, we have established baseline ex vivo frequencies of effector and Tregs at homeostasis at a population level. Copyright ©2010 by The American Association of Immunologists, Inc. All rights reserved.
Start page
5375
End page
5382
Volume
184
Issue
9
Language
English
OCDE Knowledge area
Biología celular, Microbiología
Enfermedades infecciosas
Publication version
Version of Record
Scopus EID
2-s2.0-77954496798
PubMed ID
Source
Journal of Immunology
ISSN of the container
0022-1767
Sponsor(s)
This work was supported by the Intramural Research Program of the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.
Sources of information:
Directorio de Producción Científica
Scopus