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2016 ; 13
(6
): 795-804
Nephropedia Template TP
gab.com Text
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English Wikipedia
Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions
through alternation of T helper cell polarization
#MMPMID26320740
Desrumaux C
; Lemaire-Ewing S
; Ogier N
; Yessoufou A
; Hammann A
; Sequeira-Le Grand A
; Deckert V
; Pais de Barros JP
; Le Guern N
; Guy J
; Khan NA
; Lagrost L
Cell Mol Immunol
2016[Nov]; 13
(6
): 795-804
PMID26320740
show ga
OBJECTIVE: Plasma phospholipid transfer protein (PLTP) is a key determinant of
lipoprotein metabolism, and both animal and human studies converge to indicate
that PLTP promotes atherogenesis and its thromboembolic complications. Moreover,
it has recently been reported that PLTP modulates inflammation and immune
responses. Although earlier studies from our group demonstrated that PLTP can
modify macrophage activation, the implication of PLTP in the modulation of
T-cell-mediated immune responses has never been investigated and was therefore
addressed in the present study. Approach and results: In the present study, we
demonstrated that PLTP deficiency in mice has a profound effect on CD4(+) Th0
cell polarization, with a shift towards the anti-inflammatory Th2 phenotype under
both normal and pathological conditions. In a model of contact hypersensitivity,
a significantly impaired response to skin sensitization with the
hapten-2,4-dinitrofluorobenzene (DNFB) was observed in PLTP-deficient mice
compared to wild-type (WT) mice. Interestingly, PLTP deficiency in mice exerted
no effect on the counts of total white blood cells, lymphocytes, granulocytes, or
monocytes in the peripheral blood. Moreover, PLTP deficiency did not modify the
amounts of CD4(+) and CD8(+) T lymphocyte subsets. However, PLTP-deficiency,
associated with upregulation of the Th2 phenotype, was accompanied by a
significant decrease in the production of the pro-Th1 cytokine interleukin 18 by
accessory cells. CONCLUSIONS: For the first time, this work reports a
physiological role for PLTP in the polarization of CD4(+) T cells toward the
pro-inflammatory Th1 phenotype.