CATIE IMMUNOMODULATORS: How DNCB works

IMMUNOMODULATORS: How DNCB works

TreatmentUpdate43: Vol. 4, No. 3, July 1993
Sean Hosein

DNCB may help shift the immune response from one based largely on antibody production to one where the body's CD4+ and CD8+ T-cells, macrophages and NK cells can mount sustained attacks on HIV-infected cells. CD8+ cells are " a major defense against viral infections and intracellular parasites." Keeping this arm of the immune system active appears to be increasingly important in containing HIV infection. The San Francisco researchers suggest that larger trials be done to confirm their findings. Doctors in that city and Toronto are thinking about conducting a large, observational study of DNCB in people with HIV infection.

DNCB--Notes From The 1980s

One prominent American AIDS-researcher told TreatmentUpdate that he and other doctors monitored their patients who were using DNCB in the mid-1980s. They noticed that while the CD4+ cell counts remained stable the CD8+cell counts went up. This caused the CD4/ CD8 ratio to fall. At that time some doctors felt that CD8+ cells "suppressed" the immune response and were "bad" cells. He and other physicians then discouraged their patients from further use of the drug. However, recent research in North America and the EC suggests that CD8+ cells are important, and maintaining or increasing the CD8+cell count may protect against life-threatening infections and/or cancers. He plans to analyse his patients' records to see what effect DNCB might have had on the appearance of life-threatening infections and/or cancers and survival. Further information on CD8+ cells and HIV infection will appear in a future issue of TreatmentUpdate.

DNCB Supply

The DNCB used in their experiments was supplied by HAF (Healing Alternatives Foundation) in San Francisco. DNCB is not patented by any pharmaceutical company and is thus very cheap; a DNCB kit from HAF with a 1 year supply is about $30 US and includes instructions for use. Because it is not patented there are no large profits to be made from the sale of DNCB. Thus there is no financial incentive to pay for large clinical trials of this apparently low-toxicity drug.

REFERENCES:

1. Stricker RB, Zhu YS, Elswood BF, et al. Pilot study of topical dinitrochlorobenzene (DNCB) in human immunodeficiency virus infection. Immunology Letters 1993;36:1-6.

2. Cameron PU, Forsum U, Teppler H, et al. During HIV-1 infection most blood dendritic cells are not productively infected and can induce allogenic CD4+ T-cell clonal expansion. Clinical and Experimental Immunology 1992;88:226-236.

3. Meltzer MS and Nacy CA. Delayed-type hypersensitivity and the induction of activated, cytotoxic macrophages, in Fundamental Immunology, pages 765-767. Second edition, William E. Paul editor. Raven Press, New York, 1989.

4. Erad F, Wild M-T, Gareia-Sanz JA and Le Gros G. Switch of CD8+ T cells to noncytolytic CD8 CD4 cells that make Th2 cytokines and help B cells. Science 1993;260: 1802-1805.

5. Fiala M, Kermani V and Gornbein J. Role of CD8+ in late opportunistic infections of patients with AIDS. Research in Immunology 1992;143:903-907.

6. Bird AG and Watret KC. CD8 T lymphocyte subset markers and HIV infection. Editorial Review. Clinical and Experimental Immunology 1992:90:355-356.

7. Mody CH, Chen G-H, Jackson C, et al. Depletion of murine CD8+ T cells in vivo decreases pulmonary clearance of a moderately virulent strain of Cryptococcus neoformans. Journal of Laboratory and Clinical Medicine 1993;121:765-773.

Acknowledgments:

1. We are grateful to B. Goldberg for advice, comments, support and gaining access to research, treatment activists and scientists, all of which was very helpful in understanding the complex immunology involved in writing these articles.

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