Points of control in inflammation
10.1038/nature01320
Crossref journal-article
Springer Science and Business Media LLC
Nature (297)
Bibliography

Nathan, C. (2002). Points of control in inflammation. Nature, 420(6917), 846–852.

Authors 1
  1. Carl Nathan (first)
References 113 Referenced 2,067
  1. Zweifach, B. W., Grant, L. & McCluskey, R. T. The Inflammatory Process (Academic, New York, 1965). / The Inflammatory Process by BW Zweifach (1965)
  2. Bunting, M., Harris, E. S., McIntyre, T. M., Prescott, S. M. & Zimmerman, G. A. Leukocyte adhesion deficiency syndromes: adhesion and tethering defects involving β2 integrins and selectin ligands. Curr. Opin. Hematol. 9, 30–35 (2002). (10.1097/00062752-200201000-00006) / Curr. Opin. Hematol. by M Bunting (2002)
  3. Biesma, D. H. et al. A family with complement factor D deficiency. J. Clin. Invest. 108, 233–240 (2001). (10.1172/JCI200112023) / J. Clin. Invest. by DH Biesma (2001)
  4. Soiffer, R. et al. Vaccination with irradiated autologous melanoma cells engineered to secrete human granulocyte-macrophage colony-stimulating factor generates potent antitumor immunity in patients with metastatic melanoma. Proc. Natl Acad. Sci. USA 95, 13141–13146 (1998). (10.1073/pnas.95.22.13141) / Proc. Natl Acad. Sci. USA by R Soiffer (1998)
  5. Morales, A. Intravesical therapy of bladder cancer: an immunotherapy success story. Int. J. Urol. 3, 329–333 (1996). (10.1111/j.1442-2042.1996.tb00548.x) / Int. J. Urol. by A Morales (1996)
  6. Riewald, M., Petrovan, R. J., Donner, A., Mueller, B. M. & Ruf, W. Activation of endothelial cell protease activated receptor 1 by the protein C pathway. Science 296, 1880–1882 (2002). (10.1126/science.1071699) / Science by M Riewald (2002)
  7. Steinhoff, M. et al. Agonists of proteinase-activated receptor 2 induce inflammation by a neurogenic mechanism. Nature Med. 6, 151–158 (2000). (10.1038/72247) / Nature Med. by M Steinhoff (2000)
  8. Basu, S. & Srivastava, P. K. Heat shock proteins: the fountainhead of innate and adaptive immune responses. Cell Stress Chaper. 5, 443–451 (2000). (10.1379/1466-1268(2000)005<0443:HSPTFO>2.0.CO;2) / Cell Stress Chaper. by S Basu (2000)
  9. Scaffidi, P., Misteli, T. & Bianchi, M. E. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 418, 191–195 (2002). (10.1038/nature00858) / Nature by P Scaffidi (2002)
  10. Carp, H. Mitochondrial N-formylmethionyl proteins as chemoattractants for neutrophils. J. Exp. Med. 155, 264–275 (1982). (10.1084/jem.155.1.264) / J. Exp. Med. by H Carp (1982)
  11. Muller, W. A. Leukocyte-endothelial cell interactions in the inflammatory response. Lab. Invest. 82, 521–533 (2002). (10.1038/labinvest.3780446) / Lab. Invest. by WA Muller (2002)
  12. Lee, D. M. et al. Mast cells: a cellular link between autoantibodies and inflammatory arthritis. Science 297, 1689–1692 (2002). (10.1126/science.1073176) / Science by DM Lee (2002)
  13. van der Poll, T. Coagulation and inflammation. J. Endotoxin Res. 7, 301–304 (2001). (10.1177/09680519010070040301) / J. Endotoxin Res. by T van der Poll (2001)
  14. Kaplan, A. P., Joseph, K. & Silverberg, M. Pathways for bradykinin formation and inflammatory disease. J. Allergy Clin. Immunol. 109, 195–209 (2002). (10.1067/mai.2002.121316) / J. Allergy Clin. Immunol. by AP Kaplan (2002)
  15. Nathan, C., Xie, Q. W., Halbwachs-Mecarelli, L. & Jin, W. W. Albumin inhibits neutrophil spreading and hydrogen peroxide release by blocking the shedding of CD43 (sialophorin, leukosialin). J. Cell Biol. 122, 243–256 (1993). (10.1083/jcb.122.1.243) / J. Cell Biol. by C Nathan (1993)
  16. Nathan, C. F. Neutrophil activation on biological surfaces. Massive secretion of hydrogen peroxide in response to products of macrophages and lymphocytes. J. Clin. Invest. 80, 1550–1560 (1987). (10.1172/JCI113241) / J. Clin. Invest. by CF Nathan (1987)
  17. Weiss, S. J. Tissue destruction by neutrophils. N. Engl. J. Med. 320, 365–376 (1989). (10.1056/NEJM198902093200606) / N. Engl. J. Med. by SJ Weiss (1989)
  18. Morgan, J. G., Pereira, H. A., Sukiennicki, T., Spitznagel, J. K. & Larrick, J. W. Human neutrophil granule cationic protein CAP37 is a specific macrophage chemotaxin that shares homology with inflammatory proteinases. Adv. Exp. Med. Biol. 305, 89–96 (1991). (10.1007/978-1-4684-6009-4_11) / Adv. Exp. Med. Biol. by JG Morgan (1991)
  19. Yang, D. et al. β-defensins: linking innate and adaptive immunity through dendritic and T cell CCR6. Science 286, 525–528 (1999). (10.1126/science.286.5439.525) / Science by D Yang (1999)
  20. Robbiani, D. F. et al. The leukotriene C4 transporter MRP1 regulates CCL19 (MIP-3β, ELC)-dependent mobilization of dendritic cells to lymph nodes. Cell 103, 757–768 (2000). (10.1016/S0092-8674(00)00179-3) / Cell by DF Robbiani (2000)
  21. Matzinger, P. The danger model: a renewed sense of self. Science 296, 301–305 (2002). (10.1126/science.1071059) / Science by P Matzinger (2002)
  22. Medzhitov, R. & Janeway, C. A. Jr Decoding the patterns of self and nonself by the innate immune system. Science 296, 298–300 (2002). (10.1126/science.1068883) / Science by R Medzhitov (2002)
  23. Kiechl, S. et al. Toll-like receptor 4 polymorphisms and atherogenesis. N. Engl. J. Med. 347, 185–192 (2002). (10.1056/NEJMoa012673) / N. Engl. J. Med. by S Kiechl (2002)
  24. Fink, M. P. Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability. Semin. Respir. Infect. 9, 256–260 (1994). / Semin. Respir. Infect. by MP Fink (1994)
  25. Levy, B. D., Clish, C. B., Schmidt, B., Gronert, K. & Serhan, C. N. Lipid mediator class switching during acute inflammation: signals in resolution. Nature Immunol. 2, 612–619 (2001). (10.1038/89759) / Nature Immunol. by BD Levy (2001)
  26. Mizumoto, N. et al. CD39 is the dominant Langerhans cell-associated ecto-NTPDase: modulatory roles in inflammation and immune responsiveness. Nature Med. 8, 358–365 (2002). (10.1038/nm0402-358) / Nature Med. by N Mizumoto (2002)
  27. Ohta, A. & Sitkovsky, M. Role of G-protein-coupled adenosine receptors in downregulation of inflammation and protection from tissue damage. Nature 414, 916–920 (2001). (10.1038/414916a) / Nature by A Ohta (2001)
  28. Hoek, R. M. et al. Down-regulation of the macrophage lineage through interaction with OX2 (CD200). Science 290, 1768–1771 (2000). (10.1126/science.290.5497.1768) / Science by RM Hoek (2000)
  29. Daheshia, M., Friend, D. S., Grusby, M. J., Austen, K. F. & Katz, H. R. Increased severity of local and systemic anaphylactic reactions in gp49B1-deficient mice. J. Exp. Med. 194, 227–234 (2001). (10.1084/jem.194.2.227) / J. Exp. Med. by M Daheshia (2001)
  30. Teder, P. et al. Resolution of lung inflammation by CD44. Science 296, 155–158 (2002). (10.1126/science.1069659) / Science by P Teder (2002)
  31. Ashcroft, G. S. et al. Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing. Nature Med. 6, 1147–1153 (2000). (10.1038/80489) / Nature Med. by GS Ashcroft (2000)
  32. Marino, M. W. et al. Characterization of tumor necrosis factor-deficient mice. Proc. Natl Acad. Sci. USA 94, 8093–8098 (1997). (10.1073/pnas.94.15.8093) / Proc. Natl Acad. Sci. USA by MW Marino (1997)
  33. Hodge-Dufour, J. et al. Inhibition of interferon γ induced interleukin 12 production: a potential mechanism for the anti-inflammatory activities of tumor necrosis factor. Proc. Natl Acad. Sci. USA 95, 13806–13811 (1998). (10.1073/pnas.95.23.13806) / Proc. Natl Acad. Sci. USA by J Hodge-Dufour (1998)
  34. Jin, F. Y., Nathan, C., Radzioch, D. & Ding, A. Secretory leukocyte protease inhibitor: a macrophage product induced by and antagonistic to bacterial lipopolysaccharide. Cell 88, 417–426 (1997). (10.1016/S0092-8674(00)81880-2) / Cell by FY Jin (1997)
  35. Grobmyer, S. R. et al. Secretory leukocyte protease inhibitor, an inhibitor of neutrophil activation, is elevated in serum in human sepsis and experimental endotoxemia. Crit. Care Med. 28, 1276–1282 (2000). (10.1097/00003246-200005000-00003) / Crit. Care Med. by SR Grobmyer (2000)
  36. Zhu, J. et al. Conversion of proepithelin to epithelins: roles of SLPI and elastase in host defense and wound repair. Cell (in the press).
  37. Segal, B. H., Leto, T. L., Gallin, J. I., Malech, H. L. & Holland, S. M. Genetic, biochemical, and clinical features of chronic granulomatous disease. Medicine (Baltimore) 79, 170–200 (2000). (10.1097/00005792-200005000-00004) / Medicine (Baltimore) by BH Segal (2000)
  38. Morgenstern, D. E., Gifford, M. A., Li, L. L., Doerschuk, C. M. & Dinauer, M. C. Absence of respiratory burst in X-linked chronic granulomatous disease mice leads to abnormalities in both host defense and inflammatory response to Aspergillus fumigatus. J. Exp. Med. 185, 207–218 (1997). (10.1084/jem.185.2.207) / J. Exp. Med. by DE Morgenstern (1997)
  39. Clark, R. A. & Klebanoff, S. J. Chemotactic factor inactivation by the myeloperoxidase-hydrogen peroxide-halide system. J. Clin. Invest. 64, 913–920 (1979). (10.1172/JCI109557) / J. Clin. Invest. by RA Clark (1979)
  40. Nathan, C. Inducible nitric oxide synthase: what difference does it make? J. Clin. Invest. 100, 2417–2423 (1997). (10.1172/JCI119782) / J. Clin. Invest. by C Nathan (1997)
  41. Bogdan, C. Nitric oxide and the immune response. Nature Immunol. 2, 907–916 (2001). (10.1038/ni1001-907) / Nature Immunol. by C Bogdan (2001)
  42. Schur, P. H. Genetics of complement deficiencies associated with lupus-like syndromes. Arthritis Rheum. 21, S153–S160 (1978). (10.1002/art.1780210924) / Arthritis Rheum. by PH Schur (1978)
  43. Walport, M. J., Davies, K. A., Morley, B. J. & Botto, M. Complement deficiency and autoimmunity. Ann. NY Acad. Sci. 815, 267–281 (1997). (10.1111/j.1749-6632.1997.tb52069.x) / Ann. NY Acad. Sci. by MJ Walport (1997)
  44. Wert, S. E. et al. Increased metalloproteinase activity, oxidant production, and emphysema in surfactant protein D gene-inactivated mice. Proc. Natl Acad. Sci. USA 97, 5972–5977 (2000). (10.1073/pnas.100448997) / Proc. Natl Acad. Sci. USA by SE Wert (2000)
  45. Ogura, Y. et al. Nod2, a Nod1/Apaf-1 family member that is restricted to monocytes and activates NF-κB. J. Biol. Chem. 276, 4812–4818 (2001). (10.1074/jbc.M008072200) / J. Biol. Chem. by Y Ogura (2001)
  46. Kastner, D. L. & O'Shea, J. J. A fever gene comes in from the cold. Nature Genet. 29, 241–242 (2001). (10.1038/ng1101-241) / Nature Genet. by DL Kastner (2001)
  47. Liao, J. K. Isoprenoids as mediators of the biological effects of statins. J. Clin. Invest. 110, 285–288 (2002). (10.1172/JCI0216421) / J. Clin. Invest. by JK Liao (2002)
  48. Levy, B. D. et al. Multi-pronged inhibition of airway hyper-responsiveness and inflammation by lipoxin A4 . Nature Med. 8, 1018–1023 (2002). (10.1038/nm748) / Nature Med. by BD Levy (2002)
  49. Keane, J. et al. Tuberculosis associated with infliximab, a tumor necrosis factor α-neutralizing agent. N. Engl. J. Med. 345, 1098–1104 (2001). (10.1056/NEJMoa011110) / N. Engl. J. Med. by J Keane (2001)
  50. Vaishnaw, A. K. et al. The spectrum of apoptotic defects and clinical manifestations, including systemic lupus erythematosus, in humans with CD95 (Fas/APO-1) mutations. Arthritis Rheum. 42, 1833–1842 (1999). (10.1002/1529-0131(199909)42:9<1833::AID-ANR7>3.0.CO;2-Q) / Arthritis Rheum. by AK Vaishnaw (1999)
  51. Fisher, G. H. et al. Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell 81, 935–946 (1995). (10.1016/0092-8674(95)90013-6) / Cell by GH Fisher (1995)
  52. Sneller, M. C. et al. A novel lymphoproliferative/autoimmune syndrome resembling murine lpr/gld disease. J. Clin. Invest. 90, 334–341 (1992). (10.1172/JCI115867) / J. Clin. Invest. by MC Sneller (1992)
  53. Cohen, P. L. & Eisenberg, R. A. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Annu. Rev. Immunol. 9, 243–269 (1991). (10.1146/annurev.iy.09.040191.001331) / Annu. Rev. Immunol. by PL Cohen (1991)
  54. Botto, M. et al. Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies. Nature Genet. 19, 56–59 (1998). (10.1038/ng0598-56) / Nature Genet. by M Botto (1998)
  55. Lipsker, D. M. et al. Lupus erythematosus associated with genetically determined deficiency of the second component of the complement. Arch. Dermatol. 136, 1508–1514 (2000). / Arch. Dermatol. by DM Lipsker (2000)
  56. Chen, Z., Koralov, S. B. & Kelsoe, G. Complement C4 inhibits systemic autoimmunity through a mechanism independent of complement receptors CR1 and CR2. J. Exp. Med. 192, 1339–1352 (2000). (10.1084/jem.192.9.1339) / J. Exp. Med. by Z Chen (2000)
  57. Sullivan, K. E. Complement deficiency and autoimmunity. Curr. Opin. Pediatr. 10, 600–606 (1998). (10.1097/00008480-199810060-00011) / Curr. Opin. Pediatr. by KE Sullivan (1998)
  58. Xu, C. et al. A critical role for murine complement regulator Crry in fetomaternal tolerance. Science 287, 498–501 (2000). (10.1126/science.287.5452.498) / Science by C Xu (2000)
  59. Bickerstaff, M. C. et al. Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity. Nature Med. 5, 694–697 (1999). (10.1038/9544) / Nature Med. by MC Bickerstaff (1999)
  60. Napirei, M. et al. Features of systemic lupus erythematosus in Dnase1-deficient mice. Nature Genet. 25, 177–181 (2000). (10.1038/76032) / Nature Genet. by M Napirei (2000)
  61. Bolland, S., Yim, Y. S., Tus, K., Wakeland, E. K. & Ravetch, J. V. Genetic modifiers of systemic lupus erythematosus in FcγRIIB−/− mice. J. Exp. Med. 195, 1167–1174 (2002). (10.1084/jem.20020165) / J. Exp. Med. by S Bolland (2002)
  62. Sullivan, K. E., Mullen, C. A., Blaese, R. M. & Winkelstein, J. A. A multiinstitutional survey of the Wiskott-Aldrich syndrome. J. Pediatr. 125, 876–885 (1994). (10.1016/S0022-3476(05)82002-5) / J. Pediatr. by KE Sullivan (1994)
  63. Leverrier, Y. et al. Cutting edge: the Wiskott-Aldrich syndrome protein is required for efficient phagocytosis of apoptotic cells. J. Immunol. 166, 4831–4834 (2001). (10.4049/jimmunol.166.8.4831) / J. Immunol. by Y Leverrier (2001)
  64. Snapper, S. B. et al. Wiskott-Aldrich syndrome protein-deficient mice reveal a role for WASP in T but not B cell activation. Immunity 9, 81–91 (1998). (10.1016/S1074-7613(00)80590-7) / Immunity by SB Snapper (1998)
  65. McDermott, M. F. et al. Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes. Cell 97, 133–144 (1999). (10.1016/S0092-8674(00)80721-7) / Cell by MF McDermott (1999)
  66. Shull, M. M. et al. Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease. Nature 359, 693–699 (1992). (10.1038/359693a0) / Nature by MM Shull (1992)
  67. Kulkarni, A. B. et al. Transforming growth factor β1 null mutation in mice causes excessive inflammatory response and early death. Proc. Natl Acad. Sci. USA 90, 770–774 (1993). (10.1073/pnas.90.2.770) / Proc. Natl Acad. Sci. USA by AB Kulkarni (1993)
  68. Willerford, D. M. et al. Interleukin-2 receptor α chain regulates the size and content of the peripheral lymphoid compartment. Immunity 3, 521–530 (1995). (10.1016/1074-7613(95)90180-9) / Immunity by DM Willerford (1995)
  69. Sadlack, B. et al. Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene. Cell 75, 253–261 (1993). (10.1016/0092-8674(93)80067-O) / Cell by B Sadlack (1993)
  70. Kuhn, R., Lohler, J., Rennick, D., Rajewsky, K. & Muller, W. Interleukin-10-deficient mice develop chronic enterocolitis. Cell 75, 263–274 (1993). (10.1016/0092-8674(93)80068-P) / Cell by R Kuhn (1993)
  71. Dranoff, G. et al. Involvement of granulocyte-macrophage colony-stimulating factor in pulmonary homeostasis. Science 264, 713–716 (1994). (10.1126/science.8171324) / Science by G Dranoff (1994)
  72. Nicklin, M. J., Hughes, D. E., Barton, J. L., Ure, J. M. & Duff, G. W. Arterial inflammation in mice lacking the interleukin 1 receptor antagonist gene. J. Exp. Med. 191, 303–312 (2000). (10.1084/jem.191.2.303) / J. Exp. Med. by MJ Nicklin (2000)
  73. Horai, R. et al. Development of chronic inflammatory arthropathy resembling rheumatoid arthritis in interleukin 1 receptor antagonist-deficient mice. J. Exp. Med. 191, 313–320 (2000). (10.1084/jem.191.2.313) / J. Exp. Med. by R Horai (2000)
  74. Mombaerts, P. et al. Spontaneous development of inflammatory bowel disease in T cell receptor mutant mice. Cell 75, 274–282 (1993). (10.1016/0092-8674(93)80069-Q) / Cell by P Mombaerts (1993)
  75. Waterhouse, P. et al. Lymphoproliferative disorders with early lethality in mice deficient in Ctla-4. Science 270, 985–988 (1995). (10.1126/science.270.5238.985) / Science by P Waterhouse (1995)
  76. Tivol, E. A. et al. Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4. Immunity 3, 541–547 (1995). (10.1016/1074-7613(95)90125-6) / Immunity by EA Tivol (1995)
  77. Nishimura, H., Nose, M., Hiai, H., Minato, N. & Honjo, T. Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor. Immunity 11, 141–151 (1999). (10.1016/S1074-7613(00)80089-8) / Immunity by H Nishimura (1999)
  78. Sommers, C. L. et al. A LAT mutation that inhibits T cell development yet induces lymphoproliferation. Science 296, 2040–2043 (2002). (10.1126/science.1069066) / Science by CL Sommers (2002)
  79. Alexander, W. S. et al. SOCS1 is a critical inhibitor of interferon γ signaling and prevents the potentially fatal neonatal actions of this cytokine. Cell 98, 597–608 (1999). (10.1016/S0092-8674(00)80047-1) / Cell by WS Alexander (1999)
  80. Okkenhaug, K. et al. Impaired B and T cell antigen receptor signaling in p110δ PI 3-kinase mutant mice. Science 297, 1031–1034 (2002). (10.1126/science.1073560) / Science by K Okkenhaug (2002)
  81. Di Cristofano, A. et al. Impaired Fas response and autoimmunity in Pten+/− mice. Science 285, 2122–2125 (1999). (10.1126/science.285.5436.2122) / Science by A Di Cristofano (1999)
  82. Hibbs, M. L. et al. Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease. Cell 83, 301–311 (1995). (10.1016/0092-8674(95)90171-X) / Cell by ML Hibbs (1995)
  83. Nishizumi, H. et al. Impaired proliferation of peripheral B cells and indication of autoimmune disease in lyn-deficient mice. Immunity 3, 549–560 (1995). (10.1016/1074-7613(95)90126-4) / Immunity by H Nishizumi (1995)
  84. Bachmaier, K. et al. Negative regulation of lymphocyte activation and autoimmunity by the molecular adaptor Cbl-b. Nature 403, 211–216 (2000). (10.1038/35003228) / Nature by K Bachmaier (2000)
  85. Rudolph, U. et al. Ulcerative colitis and adenocarcinoma of the colon in Gαi2-deficient mice. Nature Genet. 10, 143–150 (1995). (10.1038/ng0695-143) / Nature Genet. by U Rudolph (1995)
  86. Tsui, H. W., Siminovitch, K. A., de Souza, L. & Tsui, F. W. Motheaten and viable motheaten mice have mutations in the haematopoietic cell phosphatase gene. Nature Genet. 4, 124–129 (1993). (10.1038/ng0693-124) / Nature Genet. by HW Tsui (1993)
  87. Shultz, L. D. et al. Mutations at the murine motheaten locus are within the hematopoietic cell protein-tyrosine phosphatase (Hcph) gene. Cell 73, 1445–1454 (1993). (10.1016/0092-8674(93)90369-2) / Cell by LD Shultz (1993)
  88. Helgason, C. D. et al. Targeted disruption of SHIP leads to hemopoietic perturbations, lung pathology, and a shortened life span. Genes Dev. 12, 1610–1620 (1998). (10.1101/gad.12.11.1610) / Genes Dev. by CD Helgason (1998)
  89. Balomenos, D. et al. The cell cycle inhibitor p21 controls T-cell proliferation and sex-linked lupus development. Nature Med. 6, 171–176 (2000). (10.1038/72272) / Nature Med. by D Balomenos (2000)
  90. Taylor, G. A. et al. A pathogenetic role for TNFα in the syndrome of cachexia, arthritis, and autoimmunity resulting from tristetraprolin (TTP) deficiency. Immunity 4, 445–454 (1996). (10.1016/S1074-7613(00)80411-2) / Immunity by GA Taylor (1996)
  91. Ranger, A. M., Oukka, M., Rengarajan, J. & Glimcher, L. H. Inhibitory function of two NFAT family members in lymphoid homeostasis and Th2 development. Immunity 9, 627–635 (1998). (10.1016/S1074-7613(00)80660-3) / Immunity by AM Ranger (1998)
  92. Pasparakis, M. et al. TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2. Nature 417, 861–866 (2002). (10.1038/nature00820) / Nature by M Pasparakis (2002)
  93. The International Incontinentia Pigmenti (IP) Consortium. Genomic rearrangement in NEMO impairs NF-κB activation and is a cause of incontinentia pigmenti. Nature 405, 466–472 (2000). (10.1038/35013114)
  94. Schmidt-Supprian, M. et al. NEMO/IKKγ-deficient mice model incontinentia pigmenti. Mol. Cell 5, 981–992 (2000). (10.1016/S1097-2765(00)80263-4) / Mol. Cell by M Schmidt-Supprian (2000)
  95. Makris, C. et al. Female mice heterozygous for IKKγ/NEMO deficiencies develop a dermatopathy similar to the human X-linked disorder incontinentia pigmenti. Mol. Cell 5, 969–979 (2000). (10.1016/S1097-2765(00)80262-2) / Mol. Cell by C Makris (2000)
  96. Klement, J. F. et al. IκBα deficiency results in a sustained NF-κB response and severe widespread dermatitis in mice. Mol. Cell. Biol. 16, 2341–2349 (1996). (10.1128/MCB.16.5.2341) / Mol. Cell. Biol. by JF Klement (1996)
  97. Perry, W. L. et al. The itchy locus encodes a novel ubiquitin protein ligase that is disrupted in a18H mice. Nature Genet. 18, 143–146 (1998). (10.1038/ng0298-143) / Nature Genet. by WL Perry (1998)
  98. Weih, F. et al. Multiorgan inflammation and hematopoietic abnormalities in mice with a targeted disruption of RelB, a member of the NF-κB/Rel family. Cell 80, 331–340 (1995). (10.1016/0092-8674(95)90416-6) / Cell by F Weih (1995)
  99. Burkly, L. et al. Expression of relB is required for the development of thymic medulla and dendritic cells. Nature 373, 531–536 (1995). (10.1038/373531a0) / Nature by L Burkly (1995)
  100. Barton, D., HogenEsch, H. & Weih, F. Mice lacking the transcription factor RelB develop T cell-dependent skin lesions similar to human atopic dermatitis. Eur. J. Immunol. 30, 2323–2332 (2000). (10.1002/1521-4141(2000)30:8<2323::AID-IMMU2323>3.0.CO;2-H) / Eur. J. Immunol. by D Barton (2000)
  101. Ishikawa, H. et al. Chronic inflammation and susceptibility to bacterial infections in mice lacking the polypeptide (p)105 precursor (NF-κB1) but expressing p50. J. Exp. Med. 187, 985–996 (1998). (10.1084/jem.187.7.985) / J. Exp. Med. by H Ishikawa (1998)
  102. Finotto, S. et al. Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet. Science 295, 336–338 (2002). (10.1126/science.1065544) / Science by S Finotto (2002)
  103. Salvador, J. M. et al. Mice lacking the p53-effector gene Gadd45a develop a lupus-like syndrome. Immunity 16, 499–508 (2002). (10.1016/S1074-7613(02)00302-3) / Immunity by JM Salvador (2002)
  104. Panwala, C. M., Jones, J. C. & Viney, J. L. A novel model of inflammatory bowel disease: mice deficient for the multiple drug resistance gene, mdr1a, spontaneously develop colitis. J. Immunol. 161, 5733–5744 (1998). (10.4049/jimmunol.161.10.5733) / J. Immunol. by CM Panwala (1998)
  105. Hugot, J. P. et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 411, 599–603 (2001). (10.1038/35079107) / Nature by JP Hugot (2001)
  106. Ogura, Y. et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature 411, 603–606 (2001). (10.1038/35079114) / Nature by Y Ogura (2001)
  107. Miceli-Richard, C. et al. CARD15 mutations in Blau syndrome. Nature Genet. 29, 19–20 (2001). (10.1038/ng720) / Nature Genet. by C Miceli-Richard (2001)
  108. International Mediterranean Fever Consortium. Ancient missense mutations in a new member of the RoRet gene family are likely to cause familial Mediterranean fever. Cell 90, 797–807 (1997). (10.1016/S0092-8674(00)80539-5) / Cell by The International FMF Consortium (1997)
  109. French FMF Consortium. A candidate gene for familial Mediterranean fever. Nature Genet. 17, 25–31 (1997). (10.1038/ng0997-25)
  110. Hoffman, H. M., Mueller, J. L., Broide, D. H., Wanderer, A. A. & Kolodner, R. D. Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle–Wells syndrome. Nature Genet. 29, 301–305 (2001). (10.1038/ng756) / Nature Genet. by HM Hoffman (2001)
  111. Houten, S. M. et al. Mutations in MVK, encoding mevalonate kinase, cause hyperimmunoglobulinaemia D and periodic fever syndrome. Nature Genet. 22, 175–177 (1999). (10.1038/9691) / Nature Genet. by SM Houten (1999)
  112. Drenth, J. P. et al. Mutations in the gene encoding mevalonate kinase cause hyper-IgD and periodic fever syndrome. International Hyper-IgD Study Group. Nature Genet. 22, 178–181 (1999). (10.1038/9696) / Nature Genet. by JP Drenth (1999)
  113. Poss, K. D. & Tonegawa, S. Heme oxygenase 1 is required for mammalian iron reutilization. Proc. Natl Acad. Sci. USA 94, 10919–10924 (1997). (10.1073/pnas.94.20.10919) / Proc. Natl Acad. Sci. USA by KD Poss (1997)
Dates
Type When
Created 22 years, 8 months ago (Dec. 18, 2002, 2 p.m.)
Deposited 2 years, 3 months ago (May 18, 2023, 2:12 p.m.)
Indexed 1 hour, 4 minutes ago (Sept. 3, 2025, 5:26 a.m.)
Issued 22 years, 9 months ago (Dec. 1, 2002)
Published 22 years, 9 months ago (Dec. 1, 2002)
Published Print 22 years, 9 months ago (Dec. 1, 2002)
Funders 0

None

@article{Nathan_2002, title={Points of control in inflammation}, volume={420}, ISSN={1476-4687}, url={http://dx.doi.org/10.1038/nature01320}, DOI={10.1038/nature01320}, number={6917}, journal={Nature}, publisher={Springer Science and Business Media LLC}, author={Nathan, Carl}, year={2002}, month=dec, pages={846–852} }