Immunophysiological role and clinical implications of non-immunoglobulin soluble products of immune effector cells

Chiappelli, Francesco

doi:10.1016/s0960-5428(06)80013-6

Cited by 6 publications

(3 citation statements)

References 33 publications

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“…A rough endocrine assessment in these patients was obtained by assessing plasma cortisol levels. Despite the important limitation of this measurement, since a one‐time point determination of cortisol during a 24‐hour period hardly provides information about circadian variations, the relevance of such data lies in their ability to suggest important patterns of neuroendocrine‐immune deregulation 40. We obtained peripheral blood from subjects with OLP lesions, whose disease was clinically and verified histologically, between 10:00 a.m. and 12:00 p.m, that is, during the peak of the cortisol circadian cycle.…”

Section: Systemic Immunopathology and Psychoneuroimmunopathologymentioning

confidence: 99%

“…Patients with erosive lesions typically showed a significant ( p < 0.05) positive correlation ( r = 0.86) between the CD4/CD8 ratio and the marker of systemic immune activation serum neopterin 38. Neopterin is a product of GTP metabolism in IFN‐activated antigen‐presenting cells, which may contribute to the sympathetic‐immune interaction 40. Neopterin levels were also significantly correlated ( r = 0.87, p < 0.05) with the percent of circulating lymphocytes that express the homing receptor to the peripheral lymph nodes, CD62L 38.…”

Section: Systemic Immunopathology and Psychoneuroimmunopathologymentioning

confidence: 99%

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Psychoneuroimmunology in Oral Biology and Medicine

Prolo¹,

Chiappelli²,

Cajulis³

et al. 2002

Annals of the New York Academy of Sciences

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Rheumatoid arthritis involves psychoneuroendocrine-immunopathological comorbidities. In the stoma, patients with rheumatoid arthritis frequently show signs of periondontal disease consequent to elevated levels of crevicular proinflammatory cytokines. It is not clear whether rheumatoid arthritis may manifest in association with immunopathological manifestations of the oral soft mucosa. Oral lichen planus (OLP), first described by E. Wilson in 1859, is a T-cell-mediated inflammatory disease whose lesions characteristically lack B cells, plasma cells, immunoglobulin. or complement. It is increasingly well characterized and recognized as a model for psychoneuroimmunology research in oral biology and medicine. To date, we have shown an association between changes in hypothalamic-pituitary-adrenal (HPA) regulation, systemic markers of cellular immunity and mood states, with clinical stages of OLP (i.e., atrophic vs. erosive vs. bullous lesions). We report significant associations (p < 0.05) between the stage of OLP, HPA deregulation, and altered distribution and functional responses of naïve CD4(+) cells. We emphasize the need to study in greater details the psychoneuroendocrine-immune inter-relationships in OLP, and we propose a novel neuroimmune hypothesis for OLP.

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Section: Systemic Immunopathology and Psychoneuroimmunopathologymentioning

confidence: 99%

Section: Systemic Immunopathology and Psychoneuroimmunopathologymentioning

confidence: 99%

Psychoneuroimmunology in Oral Biology and Medicine

Prolo¹,

Chiappelli²,

Cajulis³

et al. 2002

Annals of the New York Academy of Sciences

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“…In one ment, they are not immunologically normal. Interestingly, in the hippo-in the diagnosis of HIV/AIDS, [229] now utilizing cutting edge campus and basal ganglia the HAART-treated, cognitively normal modern molecular tools specifically in the context of NeuroAIDS, group had as many activated microglia/macrophages as the pre-are ongoing. HIV-infected were followed in neurologically asymptomatic patients on patients treated with HAART may be diagnosed with HAD/ HAART.…”

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confidence: 99%

NeuroAIDS

et al. 2008

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The neurological complications of AIDS (NeuroAIDS) include neurocognitive impairment and HIV-associated dementia (HAD; also known as AIDS dementia and HIV encephalopathy). HAD is the most significant and devastating central nervous system (CNS) complications associated with HIV infection. Despite recent advances in our knowledge of the clinical features, pathogenesis, and neurobiological aspects of HAD, it remains a formidable scientific and therapeutic challenge. An understanding of the mechanisms of HIV neuroinvasion, CNS proliferation, and HAD pathogenesis provide a basis for the interpretation of the diagnostic features of HAD and its milder form, HIV-associated minor cognitive/motor disorder (MCMD). Current diagnostic strategies are associated with significant limitations, but it is hoped that the use of biomarkers may assist researchers and clinicians in predicting the onset of the disease process and in evaluating the effects of new therapies.

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