Interferon-γ and Management of Infectious Diseases
- Gabriele Baier-Bitterlich, PhD;
- Helmut Wachter, PhD; and
- Dietmar Fuchs, PhD
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
TO THE EDITOR:
We read with interest the recent report on the National Institutes of Health conference on interferon-γ in the management of infectious diseases. Aside from its use in the treatment of chronic granulomatous disease, interferon-γ is considered to be important in treating certain intracellular infections such as leishmaniasis, toxoplasmosis, and infections by atypical mycobacteria and Mycobacterium leprae [1]. These infections seem to be characterized by a preponderance of a TH2-type immune response that has a direct inhibitory effect on TH1 cells. This effect leads to interferon-γ deficiency and diminished host defense reactions in patients [2]. Recent data on interferon-γ gene or receptor “knock-out” mice support this conclusion and justify administration of interferon-γ to patients.
We do not question the usefulness of interferon-γ therapy but want to illuminate the underlying immune state that differs from the TH1/T H2 paradigm. Examination of the immune status of patients with such infections shows that their cellular immune system is highly activated. For example, increased levels of circulating interferon-γ and of the interferon-γ-inducible factor neopterin were described in patients with leishmaniasis [3] related to M. tuberculosis [4] and M. leprae [5] infection, whereby the degree of elevation correlates with the severity of the disease. In fact, TH1 cells appear to be chronically activated. Feedback regulatory mechanisms of effector cells may counteract their microbicidal abilities and could explain why these cells can no longer destroy the pathogens. Down-regulation of cell surface receptors for interferon-γ may further explain why only high doses of interferon-γ enhance the activity of effector cells such as macrophages, which are necessary for the destruction of intracellular pathogens.
Gabriele Baier-Bitterlich, PhD
Helmut Wachter, PhD
Dietmar Fuchs, PhD
University of Innsbruck; 6020 Innsbruck, Austria
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
RSS Feeds









