Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders
Identifieur interne : 000E70 ( Istex/Corpus ); précédent : 000E69; suivant : 000E71Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders
Auteurs : Angelika Buske-Kirschbaum ; Dirk H. HellhammerSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2003-05.
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Abstract
Abstract: Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin‐E hypersecretion and activation of the predominantly T‐helper‐2 (TH2)‐like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress‐induced exacerbation of atopic symptoms and may be of clinical relevance.
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DOI: 10.1111/j.1749-6632.2003.tb03153.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders</title><author><name sortKey="Buske Irschbaum, Angelika" sort="Buske Irschbaum, Angelika" uniqKey="Buske Irschbaum A" first="Angelika" last="Buske-Kirschbaum">Angelika Buske-Kirschbaum</name><affiliation><mods:affiliation>Department of Psychobiology, University of Trier, Trier, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Address for correspondence: Dr. Angelika Buske‐Kirschbaum, Department of Psychology University of Trier, Trier, Germany.</mods:affiliation></affiliation></author><author><name sortKey="Hellhammer, Dirk H" sort="Hellhammer, Dirk H" uniqKey="Hellhammer D" first="Dirk H." last="Hellhammer">Dirk H. 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Hellhammer</name><affiliation><mods:affiliation>Department of Psychobiology, University of Trier, Trier, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-05">2003-05</date><biblScope unit="volume">992</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="231">231</biblScope><biblScope unit="page" to="240">240</biblScope></imprint><idno type="ISSN">0077-8923</idno></series><idno type="istex">1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B</idno><idno type="DOI">10.1111/j.1749-6632.2003.tb03153.x</idno><idno type="ArticleID">NYAS231</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>atopic dermatitis</term><term>hypothalamic‐pituitary‐adrenal (HPA) axis</term><term>psoriasis</term><term>psychoneuroimmunology</term><term>stress</term><term>sympathetic‐adrenomedullary (SAM) system</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Abstract: Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin‐E hypersecretion and activation of the predominantly T‐helper‐2 (TH2)‐like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress‐induced exacerbation of atopic symptoms and may be of clinical relevance.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>ANGELIKA BUSKE‐KIRSCHBAUM</name><affiliations><json:string>Department of Psychobiology, University of Trier, Trier, Germany</json:string><json:string>Address for correspondence: Dr. Angelika Buske‐Kirschbaum, Department of Psychology University of Trier, Trier, Germany.</json:string></affiliations></json:item><json:item><name>DIRK H. HELLHAMMER</name><affiliations><json:string>Department of Psychobiology, University of Trier, Trier, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>atopic dermatitis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>psoriasis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypothalamic‐pituitary‐adrenal (HPA) axis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sympathetic‐adrenomedullary (SAM) system</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>psychoneuroimmunology</value></json:item></subject><articleId><json:string>NYAS231</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Abstract: Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin‐E hypersecretion and activation of the predominantly T‐helper‐2 (TH2)‐like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress‐induced exacerbation of atopic symptoms and may be of clinical relevance.</abstract><qualityIndicators><score>5.367</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1143</abstractCharCount><pdfWordCount>3447</pdfWordCount><pdfCharCount>22325</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>160</abstractWordCount></qualityIndicators><title>Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders</title><refBibs><json:item><author><json:item><name>D.Y. Leung</name></json:item></author><host><volume>105</volume><pages><last>876</last><first>860</first></pages><author></author><title>J. Allergy Clin. Immunol.</title></host><title>Atopic dermatitis: new insights and opportunities for therapeutic interventions</title></json:item><json:item><author><json:item><name>D.Y. Leung</name></json:item></author><host><volume>104</volume><pages><last>108</last><first>99</first></pages><author></author><title>J. Allergy Clin. Immunol.</title></host><title>Pathogenesis of atopic dermatitis</title></json:item><json:item><author><json:item><name>M. Boguniewicz</name></json:item></author><host><volume>9</volume><pages><last>581</last><first>577</first></pages><author></author><title>Curr. Opin. Pediatr.</title></host><title>Advances in the understanding and treatment of atopic dermatitis</title></json:item><json:item><author><json:item><name>D.J. Eedy</name></json:item></author><host><volume>145</volume><pages><last>384</last><first>380</first></pages><author></author><title>J. Dermatol.</title></host><title>What's new in atopic dermatitis? Br</title></json:item><json:item><author><json:item><name>D.Y. Leung</name></json:item></author><host><volume>44</volume><pages><last>12</last><first>1</first></pages><author></author><title>J. Am. Acad. Dermatol.</title></host><title>Cellular and immunologic mechanisms in atopic dermatitis</title></json:item><json:item><author><json:item><name>M. Grewe</name></json:item></author><host><volume>19</volume><pages><last>361</last><first>359</first></pages><author></author><title>Immunol. Today</title></host><title>A role for Th1 and Th2 cells in the immunopathogenesis of atopic dermatitis</title></json:item><json:item><author><json:item><name>A. Buske‐Kirschbaum</name></json:item></author><host><volume>70</volume><pages><last>16</last><first>6</first></pages><author></author><title>Psychother. Psychosom.</title></host><title>Psychobiological aspects of atopic dermatitis: an overview</title></json:item><json:item><author><json:item><name>D.G. Brown</name></json:item></author><host><volume>16</volume><pages><last>327</last><first>321</first></pages><author></author><title>J. Psychosom. Res.</title></host><title>Stress as a precipitant factor of eczema</title></json:item><json:item><author><json:item><name>R.M. King</name></json:item></author><host><volume>35</volume><pages><last>706</last><first>697</first></pages><author></author><title>J. Psychosom. Res.</title></host><title>Use of a diary technique to investigate psychosomatic relations in atopic dermatitis</title></json:item><json:item><author><json:item><name>A. Ehlers</name></json:item></author><host><volume>63</volume><pages><last>635</last><first>624</first></pages><author></author><title>J. Consult. Clin. Psychol.</title></host><title>Treatment of atopic dermatitis: a comparison of psychological and dermatological approaches to relapse prevention</title></json:item><json:item><author><json:item><name>L. Melin</name></json:item></author><host><volume>115</volume><pages><last>474</last><first>467</first></pages><author></author><title>Br. J. Dermatol.</title></host><title>Behavioral treatment of scratching in patients with atopic dermatitis</title></json:item><json:item><host><author></author><title>Ader, R., D.L. Felten & N. Cohen. 2000. Psychoneuroimmunology. Academic Press. San Diego.</title></host></json:item><json:item><author><json:item><name>J.H. Persoons</name></json:item></author><host><volume>95</volume><pages><last>770</last><first>765</first></pages><author></author><title>J. Allergy Clin. Immunol.</title></host><title>Increased specific IgE production in lungs after the induction of acute stress in rats</title></json:item><json:item><author><json:item><name>L.K. Singh</name></json:item></author><host><volume>13</volume><pages><last>239</last><first>225</first></pages><author></author><title>Brain Behav. Immunol.</title></host><title>Acute immobilization stress triggers skin mast cell degranulation via corticotropin releasing hormone, neurotensin and substance P: a link to neurogenic skin disorders</title></json:item><json:item><author><json:item><name>G. Schmid‐Ott</name></json:item></author><host><volume>107</volume><pages><last>177</last><first>171</first></pages><author></author><title>J. Allergy Clin. Immunol.</title></host><title>Levels of circulating CD8 (+) T lymphocytes, natural killer cells and eosinophils increase upon acute psychosocial stress in patients with atopic dermatitis</title></json:item><json:item><author><json:item><name>M.U. Goebel</name></json:item></author><host><volume>62</volume><pages><last>670</last><first>664</first></pages><author></author><title>Psychosom. Med.</title></host><title>Acute psychological stress and exercise and changes in the peripheral leukocyte adhesion expression and density</title></json:item><json:item><author><json:item><name>I.H. Paik</name></json:item></author><host><volume>26</volume><pages><last>141</last><first>139</first></pages><author></author><title>Behav. Med.</title></host><title>Psychological stress may induce increased humoral and decreased cellular immunity</title></json:item><json:item><author><json:item><name>G.P. Chrousos</name></json:item></author><host><volume>332</volume><pages><last>1362</last><first>1351</first></pages><author></author><title>N. Engl. J. Med.</title></host><title>The hypothalamus‐pituitary‐adrenal axis and immune mediated inflammation</title></json:item><json:item><author><json:item><name>E.M. Sternberg</name></json:item></author><host><volume>169</volume><pages><last>435</last><first>429</first></pages><author></author><title>J. Endocrinol.</title></host><title>Neuroendocrine regulation of autoimmune/inflammatory disease</title></json:item><json:item><author><json:item><name>G.P. Chrousos</name></json:item></author><host><volume>106</volume><pages><last>291</last><first>275</first></pages><author></author><title>J. Allergy Clin. Immunol.</title></host><title>Stress, chronic inflammation, and emotional and physical well‐being: concurrent effects and chronic sequelae</title></json:item><json:item><author><json:item><name>E.M. Sternberg</name></json:item></author><host><volume>86</volume><pages><last>2378</last><first>2374</first></pages><author></author><title>Proc. Natl. Acad. Sci. USA</title></host><title>Inflammatory mediator‐induced hypothalamic‐pituitary‐adrenal axis activation is defective in streptococcal cell wall arthritis‐susceptible Lewis rats</title></json:item><json:item><author><json:item><name>L. Tonelli</name></json:item></author><host><volume>184</volume><pages><last>211</last><first>203</first></pages><author></author><title>Immunol. Rev.</title></host><title>Neuroendocrine responses regulating susceptibility and resistance to autoimmune/inflammatory disease in inbred rat strains</title></json:item><json:item><author><json:item><name>C. Kirschbaum</name></json:item></author><host><volume>28</volume><pages><last>81</last><first>76</first></pages><author></author><title>Neuropsychobiology</title></host><title>The “Trier Social Stress Test:” a tool for investigating psychobiological stress responses in a laboratory setting</title></json:item><json:item><author><json:item><name>A. Buske‐Kirschbaum</name></json:item></author><host><volume>59</volume><pages><last>426</last><first>419</first></pages><author></author><title>Psychosom. Med.</title></host><title>Attenuated free cortisol response to psychosocial stress in children with atopic dermatitis</title></json:item><json:item><author><json:item><name>M. Rupprecht</name></json:item></author><host><volume>20</volume><pages><last>551</last><first>543</first></pages><author></author><title>Psychoneuroendocrinology</title></host><title>Cortisol, corticotropin, and β‐endorphin responses to corticotropin‐releasing hormone in patients with atopic eczema</title></json:item><json:item><author><json:item><name>M. Rupprecht</name></json:item></author><host><volume>183</volume><pages><last>105</last><first>100</first></pages><author></author><title>Dermatologica</title></host><title>Elevated glucocorticoid receptor concentrations before and after glucocorticoid treatment in atopic dermatitis</title></json:item><json:item><author><json:item><name>L. Maddox</name></json:item></author><host><volume>53</volume><pages><last>498</last><first>477</first></pages><author></author><title>Annu. Rev. Med.</title></host><title>The pathophysiology of asthma</title></json:item><json:item><author><json:item><name>H.C. Oettgen</name></json:item></author><host><volume>104</volume><pages><last>835</last><first>829</first></pages><author></author><title>J. Clin. Invest.</title></host><title>IgE in asthma and atopy: cellular and molecular connections</title></json:item><json:item><host><author></author><title>Buske‐Kirschbaum, A., K. von Auer, S. Krieger, et al. 2003. Blunted cortisol responses to psychosocial stress in asthmatic children: a general feature of atopic disease? Psychosom. Med. In press.</title></host></json:item><json:item><author><json:item><name>T. Ritz</name></json:item></author><host><volume>62</volume><pages><last>412</last><first>401</first></pages><author></author><title>Psychosom. Med.</title></host><title>Emotions and stress increase respiratory resistance in asthma</title></json:item><json:item><author><json:item><name>J. Kolbe</name></json:item></author><host><volume>106</volume><pages><last>215</last><first>211</first></pages><author></author><title>Chest</title></host><title>Influences on trends in asthma morbidity and mortality: the New Zealand experience</title></json:item><json:item><author><json:item><name>A. Buske‐Kirschbaum</name></json:item></author><host><volume>87</volume><pages><last>4251</last><first>4245</first></pages><author></author><title>J. Clin. Endocrinol. Metab.</title></host><title>Altered responsiveness of the hypothalamus‐pituitary‐adrenal axis and the sympathetic adrenomedullary system to stress in patients with atopic dermatitis</title></json:item><json:item><author><json:item><name>A.E. Calogero</name></json:item></author><host><volume>55</volume><pages><last>608</last><first>600</first></pages><author></author><title>Neuroendocrinology</title></host><title>Neurotransmitter‐induced hypothalamus‐pituitary‐adrenal axis responsiveness is defective in inflammatory disease‐susceptible Lewis rats: in vivo and in vitro studies suggesting globally defective hypothalamic secretion of corticotropin‐releasing hormone</title></json:item><json:item><author><json:item><name>A. Buske‐Kirschbaum</name></json:item></author><host><volume>129</volume><pages><last>167</last><first>161</first></pages><author></author><title>J. Neuroimmunol.</title></host><title>Stress‐induced immunomodulation is altered in patients with atopic dermatitis</title></json:item><json:item><author><json:item><name>L.B. Martin</name></json:item></author><host><volume>109</volume><pages><last>215</last><first>207</first></pages><author></author><title>Int. Arch. Allergy Immunol.</title></host><title>Eosinophils in allergy: role in disease, degranulation, and cytokines</title></json:item><json:item><author><json:item><name>A.V. Turnbull</name></json:item></author><host><volume>79</volume><pages><last>71</last><first>1</first></pages><author></author><title>Physiol. Rev.</title></host><title>Regulation of the hypothalamus‐pituitary‐adrenal axis by cytokines: actions and mechanisms of action</title></json:item><json:item><host><author></author><title>Buske‐Kirschbaum A., S. Fischbach, W. Rauh, et al. 2003. Increased responsiveness of the hypothalamus‐pituitary‐adrenal (HPA) axis to stress in newborns with atopic disposition. Submitted.</title></host></json:item><json:item><author><json:item><name>S. Mantagos</name></json:item></author><host><volume>72</volume><pages><last>216</last><first>214</first></pages><author></author><title>J. Clin. Endocrinol. Metab.</title></host><title>A simple stress test for evaluation of hypothalamus‐pituitary‐adrenal axis during the first 6 months of life</title></json:item><json:item><author><json:item><name>G. Mastorakos</name></json:item></author><host><volume>77</volume><pages><last>1694</last><first>1690</first></pages><author></author><title>J. Clin. Endocrinol. Metab.</title></host><title>Recombinant interleukin‐6 activates the hypothalamic‐pituitary‐adrenal axis in humans</title></json:item><json:item><author><json:item><name>D.D. Francis</name></json:item></author><host><volume>9</volume><pages><last>134</last><first>128</first></pages><author></author><title>Curr. Opin. Neurobiol.</title></host><title>Maternal care and the development of stress responses</title></json:item><json:item><host><author></author><title>Murison, R. & A.M. Milde. 1999. Long‐term effects of two animal stress procedures on corticosterone: models for PTSD [Abstr.]. Int. Soc. Psychoneuroendocrinol.</title></host></json:item><json:item><host><author></author><title>Varni, J.W. & J.L. Wallander. 1988. Pediatric chronic disabilities. In Handbook of Pediatric Psychology. D.K. Routh, Eds. Guilford Press. New York.</title></host></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>992</volume><publisherId><json:string>NYAS</json:string></publisherId><pages><total>10</total><last>240</last><first>231</first></pages><issn><json:string>0077-8923</json:string></issn><issue>1</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1749-6632</json:string></eissn><title>Annals of the New York Academy of Sciences</title><doi><json:string>10.1111/(ISSN)1749-6632</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>multidisciplinary sciences</json:string></wos><scienceMetrix><json:string>general</json:string><json:string>general science & technology</json:string><json:string>general science & technology</json:string></scienceMetrix></categories><publicationDate>2003</publicationDate><copyrightDate>2003</copyrightDate><doi><json:string>10.1111/j.1749-6632.2003.tb03153.x</json:string></doi><id>1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B</id><score>1.6166625</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2003</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Endocrine and Immune Responses to Stress in Chronic Inflammatory Skin Disorders</title><author xml:id="author-1"><persName><forename type="first">ANGELIKA</forename><surname>BUSKE‐KIRSCHBAUM</surname></persName><affiliation>Department of Psychobiology, University of Trier, Trier, Germany</affiliation><affiliation>Address for correspondence: Dr. Angelika Buske‐Kirschbaum, Department of Psychology University of Trier, Trier, Germany.</affiliation></author><author xml:id="author-2"><persName><forename type="first">DIRK H.</forename><surname>HELLHAMMER</surname></persName><affiliation>Department of Psychobiology, University of Trier, Trier, Germany</affiliation></author></analytic><monogr><title level="j">Annals of the New York Academy of Sciences</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="DOI">10.1111/(ISSN)1749-6632</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-05"></date><biblScope unit="volume">992</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="231">231</biblScope><biblScope unit="page" to="240">240</biblScope></imprint></monogr><idno type="istex">1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B</idno><idno type="DOI">10.1111/j.1749-6632.2003.tb03153.x</idno><idno type="ArticleID">NYAS231</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Abstract: Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin‐E hypersecretion and activation of the predominantly T‐helper‐2 (TH2)‐like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. 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Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin‐E hypersecretion and activation of the predominantly T‐helper‐2 (TH2)‐like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress‐induced exacerbation of atopic symptoms and may be of clinical relevance.</abstract><subject lang="en"><genre>keywords</genre><topic>stress</topic><topic>atopic dermatitis</topic><topic>psoriasis</topic><topic>hypothalamic‐pituitary‐adrenal (HPA) axis</topic><topic>sympathetic‐adrenomedullary (SAM) system</topic><topic>psychoneuroimmunology</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2003</date><detail type="title"><title>NEUROENDOCRINE AND NEURAL REGULATION OF AUTOIMMUNE AND INFLAMMATORY DISEASE: Molecular, Systems, and Clinical Insights</title></detail><detail type="volume"><caption>vol.</caption><number>992</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>231</start><end>240</end><total>10</total></extent></part></relatedItem><identifier type="istex">1ACF867618B61B7D28BA7E6D97E3D17D9C112E4B</identifier><identifier type="DOI">10.1111/j.1749-6632.2003.tb03153.x</identifier><identifier type="ArticleID">NYAS231</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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