Category:Immunosuppressants - Revision history

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	The category came into being with the transplantation of solid organs, and the founding observations belong to the zoologist [[wikipedia:Peter Medawar\|Peter Medawar]]. In 1942 Medawar, then at Oxford, was asked by the Glasgow burns surgeon [[wikipedia:Thomas Gibson (surgeon)\|Thomas Gibson]] to investigate why a Glaswegian woman's skin grafts from a donor were repeatedly rejected. Medawar's experiments in rabbits over the following decade established that the rejection was immunological, that it accelerated on second exposure (the second-set phenomenon), and that the response was specific to the donor; he then showed in 1953, with [[wikipedia:Rupert Billingham\|Rupert Billingham]] and [[wikipedia:Leslie Brent\|Leslie Brent]], that injecting donor cells into a fetal mouse produced lifelong tolerance to that donor's tissues, the principle of acquired immunological tolerance.<ref name="medawar1953">Billingham RE, Brent L, Medawar PB. Actively acquired tolerance of foreign cells. ''Nature''. 1953 Oct 3;172(4379):603-606. PMID 13099277.</ref> Medawar shared the 1960 Nobel Prize for the work, and the question of how to produce a comparable tolerance pharmacologically in an adult became the founding question of clinical transplantation.		The category came into being with the transplantation of solid organs, and the founding observations belong to the zoologist [[wikipedia:Peter Medawar\|Peter Medawar]]. In 1942 Medawar, then at Oxford, was asked by the Glasgow burns surgeon [[wikipedia:Thomas Gibson (surgeon)\|Thomas Gibson]] to investigate why a Glaswegian woman's skin grafts from a donor were repeatedly rejected. Medawar's experiments in rabbits over the following decade established that the rejection was immunological, that it accelerated on second exposure (the second-set phenomenon), and that the response was specific to the donor; he then showed in 1953, with [[wikipedia:Rupert Billingham\|Rupert Billingham]] and [[wikipedia:Leslie Brent\|Leslie Brent]], that injecting donor cells into a fetal mouse produced lifelong tolerance to that donor's tissues, the principle of acquired immunological tolerance.<ref name="medawar1953">Billingham RE, Brent L, Medawar PB. Actively acquired tolerance of foreign cells. ''Nature''. 1953 Oct 3;172(4379):603-606. PMID 13099277.</ref> Medawar shared the 1960 Nobel Prize for the work, and the question of how to produce a comparable tolerance pharmacologically in an adult became the founding question of clinical transplantation.

	The first medicine that gave a workable answer came from the cancer pharmacology of [[wikipedia:Gertrude B. Elion\|Gertrude Elion]] and [[wikipedia:George H. Hitchings\|George Hitchings]] at [[wikipedia:Burroughs Wellcome\|Burroughs Wellcome]], who in the early 1950s had developed [[wikipedia:Mercaptopurine\|6-mercaptopurine]] as a purine analogue antimetabolite for childhood acute lymphoblastic leukemia. In 1959 [[wikipedia:Robert Schwartz (immunologist)\|Robert Schwartz]] and [[wikipedia:William Dameshek\|William Dameshek]] at the New England Medical Center showed that 6-mercaptopurine could prevent rabbits from making antibodies against an injected foreign protein; the medicine was an immunosuppressant as well as a chemotherapeutic.<ref name="schwartz1959">Schwartz R, Dameshek W. Drug-induced immunological tolerance. ''Nature''. 1959 Jun 13;183(4676):1682-1683. PMID 13666859.</ref> [[wikipedia:Roy Calne\|Roy Calne]] at Cambridge, working from this lead, used a closely related ~~prodrug~~, [[wikipedia:Azathioprine\|azathioprine]], in combination with prednisolone, and in 1962 [[wikipedia:Joseph Murray\|Joseph Murray]] at the Peter Bent Brigham Hospital in Boston performed the first successful kidney transplant between unrelated donor and recipient. The azathioprine-prednisone combination was the standard regimen for the next twenty years.		The first medicine that gave a workable answer came from the cancer pharmacology of [[wikipedia:Gertrude B. Elion\|Gertrude Elion]] and [[wikipedia:George H. Hitchings\|George Hitchings]] at [[wikipedia:Burroughs Wellcome\|Burroughs Wellcome]], who in the early 1950s had developed [[wikipedia:Mercaptopurine\|6-mercaptopurine]] as a purine analogue antimetabolite for childhood acute lymphoblastic leukemia. In 1959 [[wikipedia:Robert Schwartz (immunologist)\|Robert Schwartz]] and [[wikipedia:William Dameshek\|William Dameshek]] at the New England Medical Center showed that 6-mercaptopurine could prevent rabbits from making antibodies against an injected foreign protein; the medicine was an immunosuppressant as well as a chemotherapeutic.<ref name="schwartz1959">Schwartz R, Dameshek W. Drug-induced immunological tolerance. ''Nature''. 1959 Jun 13;183(4676):1682-1683. PMID 13666859.</ref> [[wikipedia:Roy Calne\|Roy Calne]] at Cambridge, working from this lead, used a closely related compound, [[wikipedia:Azathioprine\|azathioprine]] (metabolically activated to 6-mercaptopurine), in combination with prednisolone, and in 1962 [[wikipedia:Joseph Murray\|Joseph Murray]] at the Peter Bent Brigham Hospital in Boston performed the first successful kidney transplant between unrelated donor and recipient. The azathioprine-prednisone combination was the standard regimen for the next twenty years.

	The transformative agent was found in soil. In 1969 the Sandoz microbiologist [[wikipedia:Jean Borel\|Jean Borel]], on a hiking holiday in the [[wikipedia:Hardangervidda\|Hardangervidda]] plateau of Norway, collected a sample of cold-climate soil for the company's broad screening programme; it yielded a fungus, ''[[wikipedia:Tolypocladium inflatum\|Tolypocladium inflatum]]'', whose secondary metabolite [[wikipedia:Ciclosporin\|cyclosporin A]] was found in 1972 to suppress T-cell-mediated immunity without the bone-marrow toxicity of azathioprine.<ref name="borel1976">Borel JF, Feurer C, Gubler HU, Stähelin H. Biological effects of cyclosporin A: a new antilymphocytic agent. ''Agents and Actions''. 1976 Jul;6(4):468-475. PMID 8969.</ref> [[Cyclosporine\|Cyclosporine]] was first given to human kidney-transplant recipients by [[wikipedia:David White (surgeon)\|David White]] and Calne at Cambridge in 1978 and was approved for clinical use in 1983; its introduction roughly doubled the one-year survival of cadaveric kidney transplants and opened the era of routine liver, heart, and lung transplantation. A second [[:Category:Calcineurin_inhibitors\|calcineurin inhibitor]], tacrolimus (FK-506), was isolated by Fujisawa from ''Streptomyces tsukubaensis'' at Mount Tsukuba in 1984 and proved both more potent and somewhat less nephrotoxic than cyclosporine. The two medicines share a final common pathway: they form a complex with intracellular immunophilins that inhibits the calcium-dependent phosphatase calcineurin and so prevents the dephosphorylation of NFAT and the subsequent transcription of the interleukin-2 gene.		The transformative agent was found in soil. In 1969 the Sandoz microbiologist [[wikipedia:Jean Borel\|Jean Borel]], on a hiking holiday in the [[wikipedia:Hardangervidda\|Hardangervidda]] plateau of Norway, collected a sample of cold-climate soil for the company's broad screening programme; it yielded a fungus, ''[[wikipedia:Tolypocladium inflatum\|Tolypocladium inflatum]]'', whose secondary metabolite [[wikipedia:Ciclosporin\|cyclosporin A]] was found in 1972 to suppress T-cell-mediated immunity without the bone-marrow toxicity of azathioprine.<ref name="borel1976">Borel JF, Feurer C, Gubler HU, Stähelin H. Biological effects of cyclosporin A: a new antilymphocytic agent. ''Agents and Actions''. 1976 Jul;6(4):468-475. PMID 8969.</ref> [[Cyclosporine\|Cyclosporine]] was first given to human kidney-transplant recipients by [[wikipedia:David White (surgeon)\|David White]] and Calne at Cambridge in 1978 and was approved for clinical use in 1983; its introduction roughly doubled the one-year survival of cadaveric kidney transplants and opened the era of routine liver, heart, and lung transplantation. A second [[:Category:Calcineurin_inhibitors\|calcineurin inhibitor]], tacrolimus (FK-506), was isolated by Fujisawa from ''Streptomyces tsukubaensis'' at Mount Tsukuba in 1984 and proved both more potent and somewhat less nephrotoxic than cyclosporine. The two medicines share a final common pathway: they form a complex with intracellular immunophilins that inhibits the calcium-dependent phosphatase calcineurin and so prevents the dephosphorylation of NFAT and the subsequent transcription of the interleukin-2 gene.

	A parallel and equally productive product of soil screening was sirolimus, isolated by [[wikipedia:Suren Sehgal\|Suren Sehgal]] at Ayerst Laboratories in 1972 from ''Streptomyces hygroscopicus'' in a soil sample collected on [[wikipedia:Easter Island\|Easter Island]]; the medicine retained the islanders' name for their island, '''Rapa Nui''', and was originally pursued as an antifungal before its immunosuppressant action was recognised.<ref name="vezina1975">Vézina C, Kudelski A, Sehgal SN. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. ''Journal of Antibiotics''. 1975 Oct;28(10):721-726. PMID 1102508.</ref> Sirolimus and its derivative everolimus inhibit the mTOR kinase, a downstream node of the IL-2 receptor pathway, and so block the proliferative response of T cells to interleukin-2 rather than its production. The mycophenolic-acid ~~prodrug~~ [[wikipedia:Mycophenolate mofetil\|mycophenolate mofetil]], a selective inhibitor of inosine monophosphate dehydrogenase in lymphocytes, was added to the transplantation pharmacopoeia in 1995.		A parallel and equally productive product of soil screening was sirolimus, isolated by [[wikipedia:Suren Sehgal\|Suren Sehgal]] at Ayerst Laboratories in 1972 from ''Streptomyces hygroscopicus'' in a soil sample collected on [[wikipedia:Easter Island\|Easter Island]]; the medicine retained the islanders' name for their island, '''Rapa Nui''', and was originally pursued as an antifungal before its immunosuppressant action was recognised.<ref name="vezina1975">Vézina C, Kudelski A, Sehgal SN. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. ''Journal of Antibiotics''. 1975 Oct;28(10):721-726. PMID 1102508.</ref> Sirolimus and its derivative everolimus inhibit the mTOR kinase, a downstream node of the IL-2 receptor pathway, and so block the proliferative response of T cells to interleukin-2 rather than its production. The morpholinoethyl ester of mycophenolic acid, [[wikipedia:Mycophenolate mofetil\|mycophenolate mofetil]], a selective inhibitor of inosine monophosphate dehydrogenase in lymphocytes, was added to the transplantation pharmacopoeia in 1995.

	The autoimmune-disease side of the category was, until the 1990s, dominated by the same agents transposed from transplantation: glucocorticoids, [[Methotrexate\|methotrexate]] (the antifolate originally developed by [[wikipedia:Sidney Farber\|Sidney Farber]] and Yellapragada Subbarow at Boston Children's Hospital in 1948 for childhood leukemia, then redeployed for psoriasis in the 1950s and for rheumatoid arthritis in the 1980s after the work of [[wikipedia:Michael Weinblatt\|Michael Weinblatt]] at the Brigham), azathioprine, hydroxychloroquine, and cyclophosphamide. The mid-1990s brought the first of the targeted biologic medicines. The [[:Category:TNF_inhibitors\|tumour necrosis factor inhibitors]], proposed as a rheumatoid-arthritis therapy on the basis of work in Marc Feldmann and Ravinder Maini's London laboratory showing that TNF-alpha was the upstream driver of synovial inflammation, were brought to clinical use as etanercept (a soluble decoy receptor, Immunex/Amgen, 1998), infliximab (a chimeric monoclonal antibody, Centocor, 1998), and the fully human [[Adalimumab\|adalimumab]] (Abbott/AbbVie, 2002).<ref name="elliott1994">Elliott MJ, Maini RN, Feldmann M, Kalden JR, Antoni C, Smolen JS, Leeb B, Breedveld FC, Macfarlane JD, Bijl H, et al. Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis. ''Lancet''. 1994 Oct 22;344(8930):1105-1110. PMID 7934491.</ref> The TNF inhibitors were the prototype for a class that has since extended through inhibitors of interleukin-1 (anakinra), interleukin-6 (tocilizumab), interleukin-17 (secukinumab), interleukin-12/23 (ustekinumab), and the small-molecule Janus kinase inhibitors (tofacitinib, baricitinib, upadacitinib).		The autoimmune-disease side of the category was, until the 1990s, dominated by the same agents transposed from transplantation: glucocorticoids, [[Methotrexate\|methotrexate]] (the antifolate originally developed by [[wikipedia:Sidney Farber\|Sidney Farber]] and Yellapragada Subbarow at Boston Children's Hospital in 1948 for childhood leukemia, then redeployed for psoriasis in the 1950s and for rheumatoid arthritis in the 1980s after the work of [[wikipedia:Michael Weinblatt\|Michael Weinblatt]] at the Brigham), azathioprine, hydroxychloroquine, and cyclophosphamide. The mid-1990s brought the first of the targeted biologic medicines. The [[:Category:TNF_inhibitors\|tumour necrosis factor inhibitors]], proposed as a rheumatoid-arthritis therapy on the basis of work in Marc Feldmann and Ravinder Maini's London laboratory showing that TNF-alpha was the upstream driver of synovial inflammation, were brought to clinical use as etanercept (a soluble decoy receptor, Immunex/Amgen, 1998), infliximab (a chimeric monoclonal antibody, Centocor, 1998), and the fully human [[Adalimumab\|adalimumab]] (Abbott/AbbVie, 2002).<ref name="elliott1994">Elliott MJ, Maini RN, Feldmann M, Kalden JR, Antoni C, Smolen JS, Leeb B, Breedveld FC, Macfarlane JD, Bijl H, et al. Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis. ''Lancet''. 1994 Oct 22;344(8930):1105-1110. PMID 7934491.</ref> The TNF inhibitors were the prototype for a class that has since extended through inhibitors of interleukin-1 (anakinra), interleukin-6 (tocilizumab), interleukin-17 (secukinumab), interleukin-12/23 (ustekinumab), and the small-molecule Janus kinase inhibitors (tofacitinib, baricitinib, upadacitinib).

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An '''immunosuppressant''' is a medicine given to suppress the immune response, whether to permit transplantation of organ or tissue, to treat an autoimmune disease, or to control an exuberant inflammatory reaction. The category includes the [[:Category:Corticosteroids|systemic glucocorticoids]], the antiproliferative antimetabolites, the calcineurin inhibitors, the mTOR inhibitors, the alkylating agents adapted from oncology, and the modern biologics that target specific cytokines and lymphocyte populations.

The category came into being with the transplantation of solid organs, and the founding observations belong to the zoologist [[wikipedia:Peter Medawar|Peter Medawar]]. In 1942 Medawar, then at Oxford, was asked by the Glasgow burns surgeon [[wikipedia:Thomas Gibson (surgeon)|Thomas Gibson]] to investigate why a Glaswegian woman's skin grafts from a donor were repeatedly rejected. Medawar's experiments in rabbits over the following decade established that the rejection was immunological, that it accelerated on second exposure (the second-set phenomenon), and that the response was specific to the donor; he then showed in 1953, with [[wikipedia:Rupert Billingham|Rupert Billingham]] and [[wikipedia:Leslie Brent|Leslie Brent]], that injecting donor cells into a fetal mouse produced lifelong tolerance to that donor's tissues, the principle of acquired immunological tolerance.<ref name="medawar1953">Billingham RE, Brent L, Medawar PB. Actively acquired tolerance of foreign cells. ''Nature''. 1953 Oct 3;172(4379):603-606. PMID 13099277.</ref> Medawar shared the 1960 Nobel Prize for the work, and the question of how to produce a comparable tolerance pharmacologically in an adult became the founding question of clinical transplantation.

The first medicine that gave a workable answer came from the cancer pharmacology of [[wikipedia:Gertrude B. Elion|Gertrude Elion]] and [[wikipedia:George H. Hitchings|George Hitchings]] at [[wikipedia:Burroughs Wellcome|Burroughs Wellcome]], who in the early 1950s had developed [[wikipedia:Mercaptopurine|6-mercaptopurine]] as a purine analogue antimetabolite for childhood acute lymphoblastic leukemia. In 1959 [[wikipedia:Robert Schwartz (immunologist)|Robert Schwartz]] and [[wikipedia:William Dameshek|William Dameshek]] at the New England Medical Center showed that 6-mercaptopurine could prevent rabbits from making antibodies against an injected foreign protein; the medicine was an immunosuppressant as well as a chemotherapeutic.<ref name="schwartz1959">Schwartz R, Dameshek W. Drug-induced immunological tolerance. ''Nature''. 1959 Jun 13;183(4676):1682-1683. PMID 13666859.</ref> [[wikipedia:Roy Calne|Roy Calne]] at Cambridge, working from this lead, used a closely related prodrug, [[wikipedia:Azathioprine|azathioprine]], in combination with prednisolone, and in 1962 [[wikipedia:Joseph Murray|Joseph Murray]] at the Peter Bent Brigham Hospital in Boston performed the first successful kidney transplant between unrelated donor and recipient. The azathioprine-prednisone combination was the standard regimen for the next twenty years.

The transformative agent was found in soil. In 1969 the Sandoz microbiologist [[wikipedia:Jean Borel|Jean Borel]], on a hiking holiday in the [[wikipedia:Hardangervidda|Hardangervidda]] plateau of Norway, collected a sample of cold-climate soil for the company's broad screening programme; it yielded a fungus, ''[[wikipedia:Tolypocladium inflatum|Tolypocladium inflatum]]'', whose secondary metabolite [[wikipedia:Ciclosporin|cyclosporin A]] was found in 1972 to suppress T-cell-mediated immunity without the bone-marrow toxicity of azathioprine.<ref name="borel1976">Borel JF, Feurer C, Gubler HU, Stähelin H. Biological effects of cyclosporin A: a new antilymphocytic agent. ''Agents and Actions''. 1976 Jul;6(4):468-475. PMID 8969.</ref> [[Cyclosporine|Cyclosporine]] was first given to human kidney-transplant recipients by [[wikipedia:David White (surgeon)|David White]] and Calne at Cambridge in 1978 and was approved for clinical use in 1983; its introduction roughly doubled the one-year survival of cadaveric kidney transplants and opened the era of routine liver, heart, and lung transplantation. A second [[:Category:Calcineurin_inhibitors|calcineurin inhibitor]], tacrolimus (FK-506), was isolated by Fujisawa from ''Streptomyces tsukubaensis'' at Mount Tsukuba in 1984 and proved both more potent and somewhat less nephrotoxic than cyclosporine. The two medicines share a final common pathway: they form a complex with intracellular immunophilins that inhibits the calcium-dependent phosphatase calcineurin and so prevents the dephosphorylation of NFAT and the subsequent transcription of the interleukin-2 gene.

A parallel and equally productive product of soil screening was sirolimus, isolated by [[wikipedia:Suren Sehgal|Suren Sehgal]] at Ayerst Laboratories in 1972 from ''Streptomyces hygroscopicus'' in a soil sample collected on [[wikipedia:Easter Island|Easter Island]]; the medicine retained the islanders' name for their island, '''Rapa Nui''', and was originally pursued as an antifungal before its immunosuppressant action was recognised.<ref name="vezina1975">Vézina C, Kudelski A, Sehgal SN. Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. ''Journal of Antibiotics''. 1975 Oct;28(10):721-726. PMID 1102508.</ref> Sirolimus and its derivative everolimus inhibit the mTOR kinase, a downstream node of the IL-2 receptor pathway, and so block the proliferative response of T cells to interleukin-2 rather than its production. The mycophenolic-acid prodrug [[wikipedia:Mycophenolate mofetil|mycophenolate mofetil]], a selective inhibitor of inosine monophosphate dehydrogenase in lymphocytes, was added to the transplantation pharmacopoeia in 1995.

The autoimmune-disease side of the category was, until the 1990s, dominated by the same agents transposed from transplantation: glucocorticoids, [[Methotrexate|methotrexate]] (the antifolate originally developed by [[wikipedia:Sidney Farber|Sidney Farber]] and Yellapragada Subbarow at Boston Children's Hospital in 1948 for childhood leukemia, then redeployed for psoriasis in the 1950s and for rheumatoid arthritis in the 1980s after the work of [[wikipedia:Michael Weinblatt|Michael Weinblatt]] at the Brigham), azathioprine, hydroxychloroquine, and cyclophosphamide. The mid-1990s brought the first of the targeted biologic medicines. The [[:Category:TNF_inhibitors|tumour necrosis factor inhibitors]], proposed as a rheumatoid-arthritis therapy on the basis of work in Marc Feldmann and Ravinder Maini's London laboratory showing that TNF-alpha was the upstream driver of synovial inflammation, were brought to clinical use as etanercept (a soluble decoy receptor, Immunex/Amgen, 1998), infliximab (a chimeric monoclonal antibody, Centocor, 1998), and the fully human [[Adalimumab|adalimumab]] (Abbott/AbbVie, 2002).<ref name="elliott1994">Elliott MJ, Maini RN, Feldmann M, Kalden JR, Antoni C, Smolen JS, Leeb B, Breedveld FC, Macfarlane JD, Bijl H, et al. Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis. ''Lancet''. 1994 Oct 22;344(8930):1105-1110. PMID 7934491.</ref> The TNF inhibitors were the prototype for a class that has since extended through inhibitors of interleukin-1 (anakinra), interleukin-6 (tocilizumab), interleukin-17 (secukinumab), interleukin-12/23 (ustekinumab), and the small-molecule Janus kinase inhibitors (tofacitinib, baricitinib, upadacitinib).

The therapeutic role of an immunosuppressant carries a corresponding therapeutic cost. The pharmacology of the calcineurin inhibitors is dominated by nephrotoxicity, hypertension, hyperkalemia, and tremor; the mTOR inhibitors by pneumonitis and impaired wound healing; the antimetabolites by myelosuppression; the biologics by reactivation of latent tuberculosis, hepatitis B, and the deep fungal mycoses, and (for some agents) by demyelinating disease and a small but characteristic excess of lymphoma. The risk-benefit assessment of an immunosuppressive regimen, particularly a long-term one in autoimmune disease where the alternative is not death but disability, is among the more demanding judgments in internal medicine.

== Classes indexed ==

By mechanism:

* [[:Category:Corticosteroids|Systemic glucocorticoids]] (the foundational immunosuppressants): [[Dexamethasone|dexamethasone]], [[Methylprednisolone|methylprednisolone]], [[Prednisolone|prednisolone]], [[Prednisone|prednisone]]
* Antimetabolites: [[Methotrexate|methotrexate]] (also indexed as [[:Category:Antifolates|antifolate]] and [[:Category:DMARDs|DMARD]]), [[wikipedia:Azathioprine|azathioprine]], [[wikipedia:Mycophenolate mofetil|mycophenolate]]
* [[:Category:Calcineurin_inhibitors|Calcineurin inhibitors]]: [[Cyclosporine|cyclosporine]], [[wikipedia:Tacrolimus|tacrolimus]]
* mTOR inhibitors (where built): [[wikipedia:Sirolimus|sirolimus]], [[wikipedia:Everolimus|everolimus]]
* Alkylating agents used outside cancer: cyclophosphamide
* [[:Category:Biologics|Biologic agents]]: [[:Category:TNF_inhibitors|TNF inhibitors]] including [[Adalimumab|adalimumab]], etanercept, and infliximab; the interleukin-pathway and lymphocyte-depleting [[:Category:Monoclonal_antibodies|monoclonal antibodies]]; the Janus kinase inhibitors
* Antimalarial-derived disease-modifying agents: [[wikipedia:Hydroxychloroquine|hydroxychloroquine]]

== Notes on scope ==

The boundary of this category is "medicine prescribed to suppress an undesired immune response, whether in transplantation or in autoimmune disease." Medicines whose principal indication is cancer chemotherapy (the alkylating agents in oncologic doses, the cytotoxic antimetabolites, the antineoplastic monoclonal antibodies) are collected under [[:Category:Antineoplastics|antineoplastics]]; the small number of agents that cross both categories, principally methotrexate and cyclophosphamide, are listed under both. The intravenous immunoglobulin preparations are not in the strict sense immunosuppressants but immunomodulators, and although they are administered for some of the same conditions they are collected under [[:Category:Immunomodulators|immunomodulators]]. Topical preparations whose principal indication is dermatologic (the topical calcineurin inhibitors tacrolimus and pimecrolimus, topical corticosteroids) are listed under the appropriate route-specific category in addition to this one.

== About these pages ==

This category page is an encyclopedia article about its subject. The actual index of medicines belonging to the category is generated automatically by the wiki engine, from category-membership declarations on the individual medicine pages, and appears at the foot of the page below the references.

== References ==

<references/>

[[Category:Medicines]]
[[Category:Immunomodulators]]
[[Category:CuratedCategoryPage]]