T cell plasticity in renal autoimmune disease

Area of Science:

• Immunology
• Nephrology
• Cellular Biology

Background:

• Rapidly progressive glomerulonephritis (GN) is characterized by immune cell infiltration, including CD4+ T cells.
• CD4+ T cell subsets, particularly Th17 cells, exhibit plasticity, allowing differentiation into various functional phenotypes.
• Understanding Th17 cell plasticity is crucial for developing targeted therapies for immune-mediated kidney diseases.

Purpose of the Study:

• To review the literature on CD4+ T cell plasticity in the context of immune-mediated kidney disease.
• To highlight the potential of targeting Th17 cell plasticity as a therapeutic strategy for glomerulonephritis.

Main Methods:

• Literature review focusing on CD4+ T cell plasticity and immune-mediated kidney disease.
• Analysis of studies investigating Th17 cell differentiation and modulation in experimental GN models.

Main Results:

• Th17 cells demonstrate plasticity, converting into pro-inflammatory Th1 or anti-inflammatory Tr1 cells.
• Experimental GN shows limited spontaneous Th17 cell plasticity.
• Anti-CD3 injection can modulate CD4+ T cell responses by inducing regulatory phenotypes and Th17 cell transdifferentiation into Tr1 cells (Tr1exTh17 cells).

Conclusions:

• Targeting Th17 cell plasticity represents a promising therapeutic avenue for glomerulonephritis.
• Modulation of Th17 cell plasticity, particularly through anti-CD3 treatment, can induce immunosuppressive effects beneficial for immune-mediated kidney diseases.