Movatterモバイル変換


[0]ホーム

URL:


Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Advertisement

Nature Immunology
  • News & Views
  • Published:

When ligand becomes receptor—tolerancevia B7 signaling on DCs

Nature Immunologyvolume 3pages1056–1057 (2002)Cite this article

CTLA-4–Ig is used to block the costimulation of T cells to interfere with their activation. This reagent may actually be working by provoking DCs to catabolize tryptophan, thereby depriving T cells and contributing to their demise.

This is a preview of subscription content,access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Access through your institution

Subscription info for Japanese customers

We have a dedicated website for our Japanese customers. Please go tonatureasia.com to subscribe to this journal.

Buy this article

  • Purchase on SpringerLink
  • Instant access to full article PDF

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Model of tolerance induction by B7-dependent signaling in DCs.

K. R.

References

  1. Lenschow, D.J., Walunas, T.L. & Bluestone, J.A.Annu. Rev. Immunol.14, 233–258 (1996).

    Article CAS PubMed  Google Scholar 

  2. Grohmann, U. et al.Nature Immunol.3, 1097–1101 (2002).

    Article CAS  Google Scholar 

  3. Mellor, A.L. & Munn, D.H.Immunol Today20, 469–473 (1999).

    Article CAS PubMed  Google Scholar 

  4. Steinman, R.M. & Nussenzweig, M.C.Proc. Natl. Acad. Sci. USA99, 351–358 (2002).

    Article CAS PubMed PubMed Central  Google Scholar 

  5. Salomon, B. & Bluestone, J.A.Annu. Rev. Immunol.19, 225–252 (2001).

    Article CAS PubMed  Google Scholar 

  6. Collins, A.V. et al.Immunity17, 201–210 (2002).

    Article CAS PubMed  Google Scholar 

  7. Mellor, A.L., Keskin, D.B., Johnson, T., Chandler, P. & Munn, D.H.J. Immunol.168, 3771–3776 (2002).

    Article CAS PubMed  Google Scholar 

  8. Munn, D.H. et al.Science297, 1867–1870 (2002).

    Article CAS PubMed  Google Scholar 

  9. Kishimoto, K. et al.J. Clin. Invest.109, 1471–1479 (2002).

    Article CAS PubMed PubMed Central  Google Scholar 

  10. Serreze, D.V. et al.J. Immunol.166, 1352–1359 (2001).

    Article CAS PubMed  Google Scholar 

  11. Mandelbrot, D.A. et al.J. Clin. Invest.107, 881–887 (2001).

    Article CAS PubMed PubMed Central  Google Scholar 

  12. Kaufman, K.A. et al.Molec. Hum. Reprod.5, 84–87 (1999).

    Article CAS PubMed  Google Scholar 

  13. Schwarz, A. et al.J. Immunol.165, 1824–1831 (2000).

    Article CAS PubMed  Google Scholar 

Download references

Author information

Author notes
  1. Erik B. Finger

    Present address: Department of Surgery, Massachusetts General Hospital, Boston, MA, 02114, USA

Authors and Affiliations

  1. UCSF Diabetes Center, UCSF School of Medicine, San Francisco, 94143, CA, USA

    Erik B. Finger & Jeffrey A. Bluestone

Authors
  1. Erik B. Finger

    You can also search for this author inPubMed Google Scholar

  2. Jeffrey A. Bluestone

    You can also search for this author inPubMed Google Scholar

Corresponding author

Correspondence toJeffrey A. Bluestone.

Rights and permissions

About this article

This article is cited by

Access through your institution
Buy or subscribe

Associated content

CTLA-4–Ig regulates tryptophan catabolismin vivo

  • Ursula Grohmann
  • Ciriana Orabona
  • Paolo Puccetti
Nature ImmunologyArticle

Advertisement

Search

Advanced search

Quick links

Nature Briefing

Sign up for theNature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox.Sign up for Nature Briefing

[8]ページ先頭

©2009-2025 Movatter.jp