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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Lck regulates IL-10 expression in memory-like Th1 cells.

Kyeorda L Kemp¹, Steven D Levin, Paul L Stein

¹Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

European Journal of Immunology

|November 10, 2010

Summary

The Src family kinase Lck regulates interleukin-10 (IL-10) production in T helper 1 (Th1) cells. Lck deficiency in Th1 cells increases IL-10, independent of other T helper cell subsets.

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Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

The Src family kinase Lck is known to influence T helper 2 (Th2) cell differentiation.
The specific role of Lck in T helper 1 (Th1) cell function remains largely unexplored.

Purpose of the Study:

To investigate the function of Lck in Th1 cell differentiation and cytokine production.
To elucidate the mechanisms by which Lck regulates Th1 cell responses.

Main Methods:

Utilized genetically modified mice lacking Lck in mature T cells (lck(-/-)).
Analyzed Th1 cell differentiation and cytokine profiles (IFN-γ, IL-10, IL-4, IL-17, Foxp3) via quantitative measurements.
Differentiated Th1 cultures from purified CD62L(+) (naïve) and memory/activated T cell subsets.
Assessed the impact of IL-12 and c-Maf on IL-10 production.

Main Results:

Lck-deficient Th1 cells maintained normal T-bet expression and interferon-gamma (IFN-γ) production.
A significant three-fold increase in IL-10 producing cells was observed in lck(-/-) Th1 cultures.
The elevated IL-10 was not associated with Th2, Th17, or Foxp3(+) regulatory T cell (Treg) markers.
IL-10 production was primarily from memory/activated T cells, not naïve cells.
IL-10 expression in Lck-deficient Th1 cells was dependent on IL-12 and correlated with elevated c-Maf.

Conclusions:

Lck plays a previously unrecognized role in suppressing IL-10 production within Th1 cells.
The absence of Lck leads to increased IL-10 in Th1 cells, particularly from the memory/activated subset.
This suggests a novel regulatory pathway for IL-10 in Th1 immunity involving Lck, IL-12, and c-Maf.