Immunology Today,vol. 8, No. 12, 1987
This, the 90th issue of Immunology Today, is the last for which I have responsibility as Editor. The seven yea,s_ sir,,-.e the journars founding have been extraordinarily stimulating. The task of guiding this journal in a decade of furious advance in so many aspects of immunology has been a continuous, sometimes daunting challenge. Yet the rewards have been constant: a growing readership, a rising citation index, and the increasingly widespread use of
Transient, local immunosuppression in recurrent vaginitis Sir, vaginitis is a common cQmplaint and treatment often does not prevent its recurrence. Vaginal infection may arise as a consequence of alterations in vaginal physiology or indigenous microbial flora, due to broadspectrum antibiotic or corticosteroid usage, diabetes or other endocrinopathies or normal pregnancy. I propose that recurring vaginitis in some women is a consequence of a transient and localized allergyi..r~x..~x.x.J n t l , u'-cu4 iI m = lm l l l.l .l .~i lnl le~./...~~l -, i~~.l~~-/ .l ~- bJ'~. .l l~U I I
360
...¢ . .-. iIiIU I ~
mediated immunity. Peripheral blood lymphocytes from many women with recurrent candidial vaginitis exhibit, during these episodes, a reduced in-vitro proliferative response to Candida albicans TM. Macrophages are required for Candida-induced lymphocyte proliferation and patients' lymphocytes are fully responsive to Candida if co-cultured with macrophages from women without vaginitis4. Furthermore, control lymphocytes become unresponsive to Candida when co-cultured with patients' macrophages but this inhibition is overcome by addition of inhibitors of prostaglandin synthesis, such as ibuprofen or indomethacin, or exogenous interleukin 2 (Ref. 5). It appears likely that in some women, in response to Candida, macrophages produce sufficient quantities of prostaglandin to inhibit lymphocyte proliferation. Macrophages can secrete prostaglandin E2 (Ref. 6), which blocks the production
our centrepage diagrams and supplements. But the greatest pleasure has been to be part of a scientific community which is excited by the possibilities in its work, confident of progress and eagerly attuned to new ideas. Immunology Today has tried to reflect and fuel that driving enthusiasm. It could not have clone so without the help and guidance of innumerable members of the community it has served. To all of those who have helped and supported the journal - as authors, advisors and subscribers - I offer my grateful thanks. Immunology Today is the product
of a team effort and it is a pleasure to acknowledge the participation of many members of Elsevier Science Publishers' staff worldwide: the editorial, production, advertising and promotion staff in Cambridge, and the customer services and marketing staff in Amsterdam and New York. As Director of Publications at Cold Spring Harbor Laboratory, New York, I shall maintain an active interest in immunology and I am confident that there will be no better way to do so than to remain a reader of Immunology Today under its new Editor.
John R. Inglis
of interleukin 2 (Refs 7, 8). This hypersensitivity, a contributory would be expected to reduce the cause, if present in the vagina during output of gamma interferon by T exposure to other allergens, or an lymphocytes9 which, in turn, would opportunistic infection secondary to impair monocyte maturation 1°.11 immunosuppression induced by unand the ingestion of Candida by related factors. These possibilities macrophages and polymorpho- should be distinguished and nuclear neutrophils. These women, appropriate prevention investigated. therefore, would have no defence against Candida overgrowth and S~en S.W~n would remain highly susceptible to recurrent infection by this organism. Departmentof Obstetricsand Gynecology,Cornell Beer and Rocklin have described UniversityMedicalCollege,New York, NY 10021, USA how an immediate hypersensitivity response can increase macrophage production of prostaglandin E2 and References inhibit T-lymphocyte responses12. A 1 Hobbs,J.R., Brigden, D., Davidson. F. transient histamine-induced immuno- et al. (1977)Proc R. Soc. Med. 70, 1. 1_121 .--.-r ~,UlJ~lL-'~biUll llldy U~ uccumng i n 2 Syverson,R.E., Buckly,H.R.and Gibian, these women. Candida, other (1979)Am. J. Obstet. Gynecol. 134, microorganisms or their products, J. 624-627 semen components or chemicals on 3 Witkin, S.S.,Yu, I.R.and Ledger,W.J. clothing, fingers, or toiletries may (1983) Am. J. Obstet. Gynecol. 147, bind to specific IgE antibodies on 809--811 mast cells and basophils which have 4 Witkin, S.S., Hirsch,J. and Ledger,W.J. accumulated at the site of allergen (1986)Am. J. Obstet. Gynecol. 155, introduction and induce a localized 790-795 immediate hypersensitivity response 5 Witkin, S.S.Am. J. Reprod. Immunol. in the vaginas of susceptible women. Microbiol. (in press) This would create conditions permit- 6 Bankhurst,A.D., Hastain, E., Goodwin, J.S.eta/. (1981) J. Lab. C/in. Med. 97, ting Candida overgrowth. 179-184 The hypothesis is supported by 7 Tilden, H.B. and Balch, C.M. (1982) the observation that long-standing J. Immunol. 129, 2469-2473 cycles of vaginal symptoms and 8 Chouaib, S., Chatenound, L., Candida infections in some of our Klatzmann, D. eta/. (1984) J. Immunol. patients stop when patients avoid 132, 1851-1857 suspected allergens, and/or initiate 9 Farrar,W.L., Johnson, H.M. and Farrar, the use of antihistamines. Such a J.J.(1981)J. Immunol. 126, 1120-1125 relationship between an allergic re- 10 Le, J., Prensky,W., Yip, Y.K. eta/. sponse and a Candida infection is (1983)1 Immunol. 131,2821-2826 suggested by the link between recur- 11 Taylor,S. and Bryson,Y.J. (1985) Immunol. 134, 1493-1497 rent oral candidiasis and the inges- J. 12 Beer,D.J.and Rocklin, R.E.(1984) tion of bananas in a woman with J. A/lergy C/in. Immunol. 73,439-452 banana hypersensitivity 13. Candida 13 Simon, M.R., Tubergen, D., Cassidy,J. infection may be the sole cause of eta/. (1979)C/in. Immunol. vaginitis in women with Candida Imrnunopathol. 14, 56--63
This, the 90th issue of Immunology Today, is the last for which I have responsibility as Editor. The seven yea,s_ sir,,-.e the journars founding have been extraordinarily stimulating. The task of guiding this journal in a decade of furious advance in so many aspects of immunology has been a continuous, sometimes daunting challenge. Yet the rewards have been constant: a growing readership, a rising citation index, and the increasingly widespread use of
Transient, local immunosuppression in recurrent vaginitis Sir, vaginitis is a common cQmplaint and treatment often does not prevent its recurrence. Vaginal infection may arise as a consequence of alterations in vaginal physiology or indigenous microbial flora, due to broadspectrum antibiotic or corticosteroid usage, diabetes or other endocrinopathies or normal pregnancy. I propose that recurring vaginitis in some women is a consequence of a transient and localized allergyi..r~x..~x.x.J n t l , u'-cu4 iI m = lm l l l.l .l .~i lnl le~./...~~l -, i~~.l~~-/ .l ~- bJ'~. .l l~U I I
360
...¢ . .-. iIiIU I ~
mediated immunity. Peripheral blood lymphocytes from many women with recurrent candidial vaginitis exhibit, during these episodes, a reduced in-vitro proliferative response to Candida albicans TM. Macrophages are required for Candida-induced lymphocyte proliferation and patients' lymphocytes are fully responsive to Candida if co-cultured with macrophages from women without vaginitis4. Furthermore, control lymphocytes become unresponsive to Candida when co-cultured with patients' macrophages but this inhibition is overcome by addition of inhibitors of prostaglandin synthesis, such as ibuprofen or indomethacin, or exogenous interleukin 2 (Ref. 5). It appears likely that in some women, in response to Candida, macrophages produce sufficient quantities of prostaglandin to inhibit lymphocyte proliferation. Macrophages can secrete prostaglandin E2 (Ref. 6), which blocks the production
our centrepage diagrams and supplements. But the greatest pleasure has been to be part of a scientific community which is excited by the possibilities in its work, confident of progress and eagerly attuned to new ideas. Immunology Today has tried to reflect and fuel that driving enthusiasm. It could not have clone so without the help and guidance of innumerable members of the community it has served. To all of those who have helped and supported the journal - as authors, advisors and subscribers - I offer my grateful thanks. Immunology Today is the product
of a team effort and it is a pleasure to acknowledge the participation of many members of Elsevier Science Publishers' staff worldwide: the editorial, production, advertising and promotion staff in Cambridge, and the customer services and marketing staff in Amsterdam and New York. As Director of Publications at Cold Spring Harbor Laboratory, New York, I shall maintain an active interest in immunology and I am confident that there will be no better way to do so than to remain a reader of Immunology Today under its new Editor.
John R. Inglis
of interleukin 2 (Refs 7, 8). This hypersensitivity, a contributory would be expected to reduce the cause, if present in the vagina during output of gamma interferon by T exposure to other allergens, or an lymphocytes9 which, in turn, would opportunistic infection secondary to impair monocyte maturation 1°.11 immunosuppression induced by unand the ingestion of Candida by related factors. These possibilities macrophages and polymorpho- should be distinguished and nuclear neutrophils. These women, appropriate prevention investigated. therefore, would have no defence against Candida overgrowth and S~en S.W~n would remain highly susceptible to recurrent infection by this organism. Departmentof Obstetricsand Gynecology,Cornell Beer and Rocklin have described UniversityMedicalCollege,New York, NY 10021, USA how an immediate hypersensitivity response can increase macrophage production of prostaglandin E2 and References inhibit T-lymphocyte responses12. A 1 Hobbs,J.R., Brigden, D., Davidson. F. transient histamine-induced immuno- et al. (1977)Proc R. Soc. Med. 70, 1. 1_121 .--.-r ~,UlJ~lL-'~biUll llldy U~ uccumng i n 2 Syverson,R.E., Buckly,H.R.and Gibian, these women. Candida, other (1979)Am. J. Obstet. Gynecol. 134, microorganisms or their products, J. 624-627 semen components or chemicals on 3 Witkin, S.S.,Yu, I.R.and Ledger,W.J. clothing, fingers, or toiletries may (1983) Am. J. Obstet. Gynecol. 147, bind to specific IgE antibodies on 809--811 mast cells and basophils which have 4 Witkin, S.S., Hirsch,J. and Ledger,W.J. accumulated at the site of allergen (1986)Am. J. Obstet. Gynecol. 155, introduction and induce a localized 790-795 immediate hypersensitivity response 5 Witkin, S.S.Am. J. Reprod. Immunol. in the vaginas of susceptible women. Microbiol. (in press) This would create conditions permit- 6 Bankhurst,A.D., Hastain, E., Goodwin, J.S.eta/. (1981) J. Lab. C/in. Med. 97, ting Candida overgrowth. 179-184 The hypothesis is supported by 7 Tilden, H.B. and Balch, C.M. (1982) the observation that long-standing J. Immunol. 129, 2469-2473 cycles of vaginal symptoms and 8 Chouaib, S., Chatenound, L., Candida infections in some of our Klatzmann, D. eta/. (1984) J. Immunol. patients stop when patients avoid 132, 1851-1857 suspected allergens, and/or initiate 9 Farrar,W.L., Johnson, H.M. and Farrar, the use of antihistamines. Such a J.J.(1981)J. Immunol. 126, 1120-1125 relationship between an allergic re- 10 Le, J., Prensky,W., Yip, Y.K. eta/. sponse and a Candida infection is (1983)1 Immunol. 131,2821-2826 suggested by the link between recur- 11 Taylor,S. and Bryson,Y.J. (1985) Immunol. 134, 1493-1497 rent oral candidiasis and the inges- J. 12 Beer,D.J.and Rocklin, R.E.(1984) tion of bananas in a woman with J. A/lergy C/in. Immunol. 73,439-452 banana hypersensitivity 13. Candida 13 Simon, M.R., Tubergen, D., Cassidy,J. infection may be the sole cause of eta/. (1979)C/in. Immunol. vaginitis in women with Candida Imrnunopathol. 14, 56--63
