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Major histocompatibility complex
Published in Gabriel Virella, Medical Immunology, 2019
Ellen Klohe, Janardan P. Pandey
MHC molecules are not designed to bind strongly hydrophobic antigens such as lipids or carbohydrates. While the response to carbohydrates is elicited with minimal or no cooperation from helper T cells, (thus circumventing the need for MHC presentation), the response to lipids and glycolipids involves presentation by a family of MHC Class I-like proteins, named CD1. The human CD1a-e molecules are encoded by closely linked non-polymorphic genes on chromosome 1. These molecules are structurally similar to Class I molecules, with an α chain composed of α1, α2 and α3 domains that is non-covalently associated with β2-microglobulin. However, the α1 and α2 domains form a deep groove lined with hydrophobic residues that bind lipid structures, rather than peptides. The CD1 family binds a broad range of lipids, but each family member preferentially binds one or more lipid classes that may be derived from a host of different microbes, including Mycobacterium tuberculosis, the lipopolysaccharides from gram-negative bacteria or lipotechoic acid from gram-positive bacteria. The CD1a-c molecules present lipid antigens to diverse unconventional αβ or γδ T cells, while CD1d proteins present antigens to NKT cells.
The Local Immune Response in Leprosy
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Jeanne Bertolli, Robert L. Modlin
The effectiveness of Langerhans cells as antigen-presenting cells, their dendritic morphology, and their ontogeny have led to speculation that they may be related to the dendritic cells of lymphoid organs. In addition, the CD1a epitope found on immature thymocytes is also found on Langerhans cells. Langerhans cells are more abundant in the epidermis of tuberculoid lesions than in lepromatous lesions,5,9 a finding that is consistent with their having a role in containing the infection. At the periphery of tuberculoid granulomas CD1+ Langerhans cells are present,9–14 but cells of this phenotype are rarely observed in the granulomas of lepromatous patients.
Non-melanoma skin cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
Stephen L. Morris, Sean Whittaker, Margaret Spittle
The total number of systems involved, age of disease onset and the presence of ‘vital organ’ involvement are the important prognostic factors in LCH. The Lahey scoring system296 where one point is allocated for each organ system involved by clinical assessment or simple laboratory investigation, is still the most widely used (Box 24.3). A CD1a radiolabelled technique has been evaluated as an adjunct to staging and diagnosis.
Chronic Recurrent Multifocal Osteomyelitis (CRMO): A Study of 12 Cases from One Institution and Literature Review
Published in Fetal and Pediatric Pathology, 2022
Eric Chang, Jasmine Vickery, Nadeen Zaiat, Eman Sallam, Abdul Hanan, Scott Baker, Mohamed Alhamar, Janet Poulik, Ereny Demian, Bahig M Shehata
Our biopsies revealed no associated soft tissue response. No microorganisms were identified, confirmed by negative bacterial, fungal, and mycobacterial cultures. All lesions were negative for CD1a, precluding Langerhans cell histiocytosis. The final diagnosis was determined collectively by the radiologist, pathologist, pediatrician, and infectious disease physician after correlating the clinical presentation, radiological, and bone biopsy findings. Once the correct diagnosis was rendered patients were treated with anti-inflammatory medication and steroids. Treatment plan and duration varied, but had an average duration of 6 months. Our patient cohort was followed over a span of 7 months to 6.5 years. 9 of these patients responded to therapeutic interventions with complete healing. The other 3 had recurrent lesions, including at the same sites, after a variable length of remission.
Targeting the tumor microenvironment in cholangiocarcinoma: implications for therapy
Published in Expert Opinion on Investigational Drugs, 2021
DCs function as antigen-presenting cells (APCs) which play an integral role in activation of the adaptive immune response. DCs are broadly categorized into two subsets: classical or conventional DCs (cDCs) and plasmacytoid DCs (pDC). cDCs originate from bone marrow precursors and have potent phagocytic properties [36]. In the TME, DCs activate the T cell response by capturing, processing, and cross-presenting neoantigens. However, tumor cells can transform DCs to an immature, immunosuppressive phenotype [37]. In CCA, infiltration of mature CD83+ DCs correlated with aggregation of CD4+/CD8+ T cells in the peritumoral region [38]. The presence of CD83+ DCs was also associated with improved patient outcomes. In contrast, the presence of CD1a (immature) DCs in the central tumor region is associated with a paucity of CD4+/CD8+ T cells [38]. FcεRI, a high-affinity immunoglobulin E receptor, is employed by DCs for cross presentation and priming of CTLs [39]. There is a significant decrease in FcεRI+ monocytes and DCs in the peripheral blood of patients with CCA [40]. These findings indicate that DCs are dysfunctional in CCA and unable to restrain tumor progression.
Smoking-associated interstitial lung disease: update and review
Published in Expert Review of Respiratory Medicine, 2020
Yaser T Dawod, Noah E Cook, William B Graham, Farah Madhani-Lovely, Choua Thao
PLCH is a rare condition primarily affecting young adults with no gender predominance. While there is no clear data regarding the prevalence of the disease, it is estimated PLCH accounts for 3% to 5% of adults with diffuse parenchymal lung disease [54]. Cigarette smoke stimulates the accumulation of dendritic (Langerhans) cells in the lung parenchyma and suppresses normal mechanisms of apoptosis in these cells [55]. Histopathologic findings show clusters of Langerhans cells surrounding small bronchioles which obstruct the bronchiolar walls [56]. Extension of cells to the surrounding parenchyma results in an appearance of the stellate lesions, which is characteristic of the disease [57]. The Langerhans cell expresses CD1a, S100 protein, and CD 207, which is pathognomonic of PLCH [56].