A history of latex allergy.

Archaeologists have found that latex items were used as early as 1600 BC, but it took until approximately 1900 AD before surgical gloves were commonly used. Descriptions of apparent allergic reactions to natural rubber appeared in the medical literature in 1927, and irritant and delayed-contact reactions were reported in 1933. Although irritant and delayed-contact reactions to rubber products were increasingly recognized, immediate-type allergic reactions were not reported again until 1979. However, after 1980, increasing numbers of contact urticarial reactions to latex were reported, and investigations suggested that many of these reactions were IgE-mediated. In 1984, the first anaphylactic reactions caused by latex surgical gloves were reported, followed in 1991 by the first report of a fatal anaphylactic reaction to latex. Increasing recognition of latex allergy led to divergent paths of investigation. Critical early questions were whether the observed reactions were truly IgE-mediated, and if they were IgE-mediated, what was the source of the allergen? If the allergen was present in latex products, where did it come from? Was it present in raw latex or was it added during processing? As knowledge about the allergens improved, efforts were made to develop and test materials for skin testing and for allergen-specific IgE assays. Now more than 10 unique proteins are recognized as major latex allergens. Although much has been learned about latex allergy, important unanswered questions remain, including the sources of latex exposure that led to sensitization, why latex allergy increased dramatically during the 1980s, and the prevalence of latex allergy in diverse populations. This review concentrates on the history of latex use in medicine and the dramatic emergence of immediate-type latex allergy.

Delayed type hypersensitivity: current theories with an historic perspective.

Although the delayed type hypersensitivity (DTH) reaction was discovered over 100 years ago, the exact nature of the reaction has been the subject of contentious debate over the years. The reaction was discovered in 1882 by Robert Koch, but it was not until the 1940s that Landsteiner and Chase proved that the reaction was mediated by the cellular and not the humoral arm of the immune system. The first DTH reaction described used only the tuberculin antigen (tuberculin reaction), but the definition was later expanded to include cell mediated reactions to other bacterial and viral antigens, responses to pure protein with adjuvant or haptens, and host responses to allograft. The DTH skin test is used to test if prior exposure to an antigen has occurred. When small quantities of antigen are injected dermally, a hallmark response is elicited which includes induration, swelling and monocytic infiltration into the site of the lesion within 24 to 72 hours. This reaction has been shown to be absolutely dependent on the presence of memory T cells. Both the CD4+ and CD8+ fractions of cells have been shown to modulate a response. Contemporary debate regarding the reaction is focused on the role of the Th1 and Th2 cells originally discovered by Mosmann. It has been postulated that the Th1 cell is the "inducer" of a DTH response since it secretes interferon gamma (IFN ), a potent stimulator of macrophages, while the Th2 cell is either not involved or acting as a downregulator of the cell mediated immune response. Despite the early experimental success of this theory, experiments have shown that Th2 cells may be involved in certain types of proinflammatory cell mediated immunity. This review focuses on the nature of the different forms of DTH that can be elicited and the different experimental evidence that has led to the current theories regarding DTH and its role in cell mediated immunity.