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Updated: Aug 18, 2026

T and B Cell Receptor Immune Repertoire Analysis using Next-generation Sequencing
Published on: January 12, 2021
Analysis of T cell receptor (TCR) BV-gene clonotypes in NC/Nga mice developing dermatitis resembling human atopic
Akihiro Matsuoka1, Tomohiro Kato, Yoshinao Soma
1Department of Dermatology, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki 216-8511, Japan.
Background:
Our previous study showed that T cells in skin lesions of human atopic dermatitis (AD) had oligoclonal accumulation, indicating the involvement of antigen-specific immune reactions at those sites. Recently, NC/Nga mice, which develop skin lesions similar to AD, have been proposed as a model for that disease.
Objective:
To clarify whether NC/Nga mice are suitable as a model for human AD from the viewpoint of their antigen-specific immune responses.
Methods:
Reverse transcription-polymerase chain reaction (RT-PCR) and single strand conformation polymorphism (SSCP) analyses were conducted to detect TCR BV genes of clonally expanded T cells derived from NC/Nga mice at an early phase of the AD-like dermatitis, at a late phase of the dermatitis, and with no AD-like dermatitis.
Results:
(1) T cells with TCR BV 7, 10 and 17 reside in the skin of NC/Nga mice without the AD-like dermatitis. (2) T cells with these BV genes contain oligoclonal accumulations, however, expanded T cell clonotypes are also detected in the spleen and exist constantly during the course of the AD-like dermatitis. (3) Development of the AD-like dermatitis is associated with additional oligoclonal expansion/accumulation of T cells with TCR BV 2, 4 and 6 genes. (4) Progression of the AD-like dermatitis is associated with further oligoclonal expansion/accumulation of T cells with the TCR BV 14 gene. (5) Some of the expanded TCR clonotypes are common between the individual mice and between early and late phases.
Conclusions:
Taking these data together with the previous human AD studies, NC/Nga mice seem to be an appropriate model for human AD.
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