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Updated: Mar 25, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
CD4+ T-cell subsets in inflammatory diseases: beyond the Th1/Th2 paradigm
Kiyoshi Hirahara1, Toshinori Nakayama2
1Department of Advanced Allergology of the Airway, Graduate School of Medicine, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan.
CD4(+) T-helper cells, beyond the Th1/Th2 balance, drive immune-mediated inflammatory diseases. New models highlight pathogenic T-helper populations in diseases like multiple sclerosis, psoriasis, and asthma.
Area of Science:
- Immunology
- Cellular Biology
Background:
- CD4(+) T cells are vital for immune responses and inflammatory disease pathogenesis.
- Beyond T-helper 1 (Th1) and T-helper 2 (Th2) cells, subsets like Th17, Th9, T follicular-helper (Tfh), and T-regulatory (Treg) cells are increasingly recognized.
Purpose of the Study:
- To review the contribution of diverse T-helper cell subsets to immune-mediated inflammatory diseases.
- To explore the roles of these subsets in multiple sclerosis, psoriasis, and asthma.
- To discuss the plasticity and heterogeneity of T-helper cell subsets.
Main Methods:
- Review of current literature on T-helper cell subsets.
- Analysis of T-helper cell classification based on transcription factor expression.
- Discussion of molecular mechanisms driving T-helper cell plasticity.
Main Results:
- T-helper cell subsets exhibit heterogeneity, classified by transcription factor expression.
- Memory-type Th2 cells contribute to chronic type-2 immune diseases.
- Multiple T-helper subsets are implicated in multiple sclerosis, psoriasis, and asthma.
Conclusions:
- The Th1/Th2 balance model is insufficient to explain immune-mediated inflammatory diseases.
- A pathogenic T-helper population disease-induction model is proposed for disease induction and persistence.
- Understanding T-helper cell heterogeneity is crucial for disease etiology.
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