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[Study of the humoral immune suppression of recombinant human collagen type II peptide 250-270]. | LitMetric

[Study of the humoral immune suppression of recombinant human collagen type II peptide 250-270].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Department of Clinical Immunology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.

Published: November 2006

AI Article Synopsis

  • The study aimed to examine how oral administration of the rhC II 250-270 peptide affects the humoral immune response in mice.
  • Using ELISA and ELISPOT methods, researchers measured specific antibodies and spleen cell responses in the mice after feeding them the peptide.
  • Results showed that the peptide significantly suppressed antibody production and spleen cell activity compared to the collagen-induced arthritis control group, suggesting its potential for developing treatments for rheumatoid arthritis.

Article Abstract

Aim: To investigate the modulation of rhC II 250-270 peptide on special humoral immune response in the course of oral administration.

Methods: ELISA was used to determine antigen-specific antibodies in mice sera. The frequency of anti-C II and anti-C II (250-270) antibody-forming spleen cells was measured by ELISPOT.

Results: The level of C II- and C II (250-270)- specific IgG in serum from the mice fed with rhC II (250-270) were (0.82+/-0.02) and (0.84+/-0.04) respectively, and lower significantly than those of collagen-induced arthritis (CIA) control group. The anti-C II (250-270) antibody responses were suppressed obviously (P<0.01). The frequency of antibody-forming cells in the spleen from rhC II (250-270)-fed mice were (158+/-9 counts/well) and (181+/-10 counts/well) respectively, and also were reduced significantly when compared with that in CIA control group (247+/-16 counts/well)(P<0.05).

Conclusion: Oral rhC II (250-270) could induce specific suppression of humoral responds in CIA. These findings together with a better understanding of the mechanisms of oral tolerance and regulation of humoral immune response in CIA, will help the development of innovative therapeutic intervention for rheumatoid arthritis.

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