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T cell-specific STAT3 deficiency abrogates lupus nephritis.

N Yoshida^1,2, F He¹, V C Kyttaris^1,2

¹Division of Rheumatology, Beth Israel Deaconess Medical Center, Division of Rheumatology, Boston, USA.

|September 26, 2019

Summary

Targeting Signal transducer and activator of transcription 3 (STAT3) in T cells may treat lupus nephritis. Silencing STAT3 in T cells prevented autoimmune disease development and reduced autoantibodies in mouse models.

Keywords:

SLE STAT3 T cells murine lupus nephritis

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Area of Science:

Immunology
Molecular Biology
Nephrology

Background:

Signal transducer and activator of transcription 3 (STAT3) is crucial for T-cell responses to cytokines and chemokines.
Elevated STAT3 activation is observed in T cells of patients with systemic lupus erythematosus (SLE).
STAT3 mediates T-cell migration and T:B cell interactions, contributing to SLE pathogenesis.

Purpose of the Study:

To investigate the role of STAT3 in T-cell pathophysiology within lupus nephritis.
To evaluate STAT3 as a potential therapeutic target for lupus nephritis.

Main Methods:

Utilized a CD4-driven CRE-Flox model to specifically silence STAT3 expression in T cells.
Assessed disease development, including lymphadenopathy, splenomegaly, and glomerulonephritis, in STAT3-deficient lupus-prone mice.
Employed a nephrotoxic serum model to evaluate the impact of T cell-specific STAT3 silencing on nephritis.

Main Results:

Lupus-prone mice lacking STAT3 in T cells did not develop key autoimmune symptoms like lymphadenopathy, splenomegaly, or glomerulonephritis.
Production of anti-dsDNA antibodies was significantly reduced in mice with silenced T-cell STAT3.
T cell-specific STAT3 silencing ameliorated kidney damage in the nephrotoxic serum model of nephritis.

Conclusions:

T cell-specific STAT3 silencing effectively hinders the development of autoimmune nephritis in mouse models.
STAT3 inhibition in T cells impairs their ability to support autoantibody production by B cells and reduces tissue infiltration.
Targeting STAT3 in T cells presents a promising therapeutic strategy for SLE, particularly lupus nephritis.