Immune‐Neuroendocrine Interactions and Autoimmune Diseases

Abstract

The relationship between immune-neuroendocrine system is firmly established. The messengers of this connection are hormones, neuropeptides, neurotransmitters and cytokines. The immune-neuroendocrine system have the capacity to synthesize and release these molecules, which, in turn, can stimulate or suppress the activity of immune or neuroendocrine cells by binding to receptors. In fact, hormones, neuropeptides and neurotransmitters participate in innate and adaptive immune response.Autoimmune rheumatic diseases (ARD) are characterized by aberrant production of pro-inflammatory cytokines, which are a potent activator of the HPA axis. In consequence, high levels of pro-inflammatory hormones such as estrogens and prolactin, and low levels of glucocorticoids, an anti-inflammatory hormone, have been described in the active phase of ARD. In addition, high levels of pro-inflammatory hormones and cytokines have also been frequently detected in organ involvement of patients with ARD, suggesting an abnormal local neuroendocrine immune interaction. There is evidence that hormonal changes may appear before the symptomatic phase of the disease. Therefore, it is possible that a pro-inflammatory hormone favors the rupture of tolerance, which is a key feature of autoimmune diseases. The interactions between the immune-neuroendocrine system have a major impact on our understanding of the pathogenic mechanisms, diagnosis and therapy of ARD.

Profil lesi oral pada penderita penyakit autoimun

“…Sistem kekebalan yang seharusnya berfungsi sebagai pelindung tubuh mengalami kelainan sehingga tidak dapat membedakan antara benda asing yang harus dimusnahkan dengan jaringan tubuh sendiri yang bermanfaat untuk kelangsungan hidup. [1][2][3] Penyebab penyakit autoimun belum diketahui secara pasti, namun perjalanan penyakit ini dapat akut atau kronis dan terdapat masa remisi atau Maj Ked Gi Ind. Desember 2016; 2(3): 147-154 ISSN 2460-0164 (print) ISSN 2442-2576 (online) eksaserbasi yang disertai dengan perubahan level autoantibodi dalam tubuh.…”

“…Kombinasi faktor predisposisi genetik dan faktor lingkungan diketahui melalui berbagai referensi berkontribusi terhadap perkembangan penyakit autoimun. [1][2][3][4][5] Lesi oral biasa ditemukan pada penderita penyakit autoimun sebagai manifestasi penyakit atau efek samping pengobatan. Penyakit autoimun yang dapat bermanifestasi pada rongga mulut di antaranya adalah Sistemic Lupus Erythematous (SLE), Lichen Planus, Pem gus dan Pem goid.…”

Epidemiologic Features of Appendicitis

“…Whether this has any relationship to the high incidence of autoimmune diseases like systemic lupus erythematosus, Grave's disease, multiple sclerosis and myasthenia gravis being predominant in women in this age group is not clear. Since the 17-ketosteroids estrogen and progesterone have been implicated in the modulation of the immunosuppressive state of pregnancy, it maybe that different levels of estrogens and androgens between boys and girls may be responsible for this observed difference in incidence (Ben-Hur, et al, 1995;Jara, et al, 2006;Zen, et al, 2010). Furthermore, antigenpresenting cells which play key roles in innate and adaptive immunity as well as tolerance have been found to express estrogen receptors on their surface implying that their functions may be modulated by sex hormones and would explain the purported immunological dimorphism between genders (Bouman, et al, 2005;Kovats & Carreras, 2008).…”

Alexithymia and immunoendocrine parameters in patients affected by systemic lupus erythematosus and rheumatoid arthritis

“…Attraverso le alterazioni di parametri biologici, della funzione immunitaria e di costrutti psicologici e psicopatologici, ci siamo interrogati, così come in precedenza altri autori (8,10), sulle possibili relazioni tra il costrutto alessitimico e il sistema immunitario. Studi recenti sulle interazioni tra sistema neuroendocrino e immunitario indicano che gli ormoni svolgono un ruolo importante nella patogenesi delle malattie autoimmuni, e possono essere coinvolti nella alterata risposta allo stimolo lesivo che induce la flogosi, con il conseguente sviluppo della malattia infiammatoria cronica (11). È stato, infatti, dimostrato che alterazioni del circolo funzionale neuroendocrino-immmunitario, possono contribuire alla patogenesi di malattie autoimmuni in modelli animali sperimentali (12,13).…”