517 research outputs found
Hinks, N T, NX20583
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/392471Surname: HINKS. Given Name(s) or Initials: N T. Military Service Number or Last Known Location: NX20583. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 2883.210241
Item: [2016.0049.24764] "Hinks, N T, NX20583
MR1 (in mouse and man)
No full textMR1 (major histocompatibility complex (MHC)-related protein 1) is a nonpolymorphic class Ib antigen presenting molecule recognized by the innate-like mucosal-associated invariant T cell subset. MR1 is highly conserved across all mammals, implying an essential role in host defense. It presents nonprotein antigens which include precursors and derivatives from highly conserved microbial biosynthetic pathways of riboflavin and folic acid metabolism. MR1 was identified in 1995 by degenerate PCR on human chromosome 1q25. MR1 is ubiquitously expressed across tissues, at relatively high abundance, but with virtually no detectable constitutive surface expression. MR1 has a standard MHC-I fold, with ?1 and ?2 helices forming an exposed antigen-binding cleft, held open by several bulky side chains, with a ?-sheet floor. MR1 ligands include formylpterins, naturally occurring photodegradation products of folic acid (vitamin B9), and ribityllumazines, precursors and derivatives of vitamin B2. MR1 predominantly exists in the late endoplasmic reticulum (ER), trafficking through the late endosomal and lysosomal compartments where it binds ligand, facilitated by chaperones from the MHC-II pathway: the invariant chain and HLA-DM. Diseases associated with MR1 deficiencies or polymorphisms are yet to be described, but are likely to produce predisposition to multisystem invasive infections, or chronic autoimmune inflammatory diseases
R v Hinks [2001] 1 AC 241, House of Lords
No full textEssential Cases: Criminal Law provides a bridge between course textbooks and key case judgments. This case document summarizes the facts and decision in R v Hinks [2001] 1 AC 241, House of Lords. The document also included supporting commentary from author Jonathan Herring.</p
MAIT cells in autoimmunity, immune mediated diseases and airways disease
No full textMucosal associated invariant T (MAIT) cells are a novel class of innate-like T cells, expressing a semi-invariant T cell receptor and able to recognize small molecules presented on the non-polymorphic MHC-related protein 1. Their intrinsic effector-memory phenotype, enabling secretion of pro-inflammatory cytokines, and their relative abundance in humans implies a significant potential to contribute to autoimmune processes. However, as MAIT cells were unknown until recently and specific immunological tools were unavailable, to date little is known of their roles in disease. Here I review observations from clinical studies and animal models of autoimmune and immune mediated diseases including the roles of MAIT cells in systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and airways diseases. MAIT cell deficiencies are frequently observed in peripheral blood, and at sites of disease such as the airways in asthma. However MAIT cells have a specific sensitivity to suppression by therapeutic corticosteroids that may confound many of these observations, as may the tendency of the surface marker CD161 to activation-induced down-regulation. Nonetheless the dependence on bacteria for the development of MAIT cells suggests a potentially important protective role linking the influences of early life microbial exposures and subsequent development of autoimmunity. Conversely MAIT cells could contribute to chronic inflammation either through TCR-independent activation, or potentially by TCR recognition of as-yet undiscovered ligands. Future research will be greatly facilitated by the immunological tools now available, including murine genetic models and human and murine specific tetramers
A Multilateral Decomposition of Racial Wage Differentials in the 1994 South African Labour Market
No full textThis article develops a new multilateral decomposition procedure for the analysis of wage differentials and applies this to the racial wage hierarchy in the South African labour market. Using micro-data on male workers from the 1994 October Household survey, it is found that whites received the highest wages followed by Asians, then coloureds and finally blacks. Productivity differences are shown to explain approximately two-thirds of the white and black wage differentials, with the unexplained residuals attributable to discriminatory overpayment of whites and underpayment of blacks, and virtually all of the Asian and coloured differentials. The results provide the basis for a discussion of post-apartheid policy initiatives to tackle racial inequalities in the labour market.South Africa, Race, Racial wage differentials, Race discrimination, Wage discrimination, 1994 October Household Survey, Apartheid legacy,
Letters to the Editor. Reduced numbers and proapoptotic features of mucosal-associated invariant T Cells as a characteristic finding in patients with inflammatory bowel disease
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Regulatory T cells are expanded in blood and disease sites in patients with tuberculosis
No full textRationale: T-cell responses during tuberculosis (TB) help contain Mycobacterium tuberculosis in vivo but also cause collateral damage to host tissues. Immune regulatory mechanisms may limit this immunopathology, and suppressed cellular immune responses in patients with TB suggest the presence of regulatory activity. CD4+CD25high regulatory T cells mediate suppressed cellular immunity in several chronic infections but have not been described in TB.Objective: To determine whether regulatory T cells are increased in patients with TB and whether they suppress cellular immune responses.Methods: We compared the frequency of circulating regulatory T cells in 27 untreated patients with TB and 23 healthy control subjects using two specific markers: cell-surface CD25 expression and FoxP3 mRNA expression in peripheral blood mononuclear cells.Measurements and Main Results: We detected a threefold increase in the frequency of CD4+CD25high T cells (p < 0.001) and a 2.2-fold increase in FoxP3 expression (p = 0.006) in patients with TB, and there was a positive correlation between these markers (r = 0.58, p < 0.001). Increased expression of interleukin-10 and transforming growth factor-beta1 mRNA was also detected in patients with TB but did not correlate with regulatory T-cell markers. Ex vivo depletion of CD4+CD25high cells from peripheral blood mononuclear cells resulted in increased numbers of M. tuberculosis antigen–specific IFN-{gamma}–producing T cells in seven of eight patients with TB (p = 0.005). Finally, FoxP3 expression was increased 2.3-fold in patients with extrapulmonary TB compared with patients with purely pulmonary TB (p = 0.01) and was amplified 2.6-fold at disease sites relative to blood (p = 0.043).Conclusions: Regulatory T cells are expanded in patients with TB and may contribute to suppression of Th1-type immune responses
Steroid-induced deficiency of mucosal-associated invariant T cells in the chronic Obstructive Pulmonary Disease lung: Implications for Nontypeable <i>Haemophilus influenzae</i> Infection
No full textRationale: Mucosal associated invariant T (MAIT) cells are a recently-described, abundant, pro-inflammatory T cell subset with unknown roles in pulmonary immunity. Non-typeable Haemophilus influenzae (NTHi) is the leading bacterial pathogen during COPD exacerbations and a plausible target for MAIT cells.Objectives: To investigate whether MAIT cells respond to NTHi and the effects of inhaled corticosteroids on their frequency and function in COPD. Methods: 11 participants with COPD receiving inhaled corticosteroids (ICS), 8 with steroid-naïve COPD and 21 healthy controls underwent phlebotomy, sputum induction, bronchoalveolar-lavage and endobronchial biopsy. Pulmonary and monocyte-derived macrophages were cultured in vitro with NTHi. Measurements: Frequencies of Va7.2+CD161+ MAIT cells, surface expression of MHC-related protein 1 (MR1) and intracellular IFN-y expression were measured by flow cytometry.Main Results: MAIT cell frequencies were reduced in peripheral blood in ICS-treated COPD (median 0.38% (IQR, 0.25-0.96) compared with health (1.8% (IQR, 1.4-2.5), P=0.001)) or steroid-naïve COPD (1.8% (1.2-2.3), P=0.04). MAIT cells were reduced in bronchial biopsies in steroid-treated COPD (0.73% (0.46-1.3)) compared with health (4.0% (1.6-5.0), P=0.02). Co-culture of live NTHi increased macrophage surface expression of MR1 and induced IFN-? from CD4 cells and CD8 cells, but most potently from MAIT cells (median IFN-y positive frequencies 2.9%, 8.6% and 27.6% respectively). In vitro fluticasone and budesonide reduced MR1 surface expression 2-fold and decreased NTHi-induced IFN-y secretion 8-fold.Conclusions: MAIT cells are deficient in blood and bronchial tissue in steroid-treated, but not steroid-naïve COPD. NTHi constitutes a target for pulmonary MAIT cell immune responses, which are significantly impaired by corticosteroids.<br/
Rapid diagnosis of CNS tuberculosis by a T-cell interferon-gamma release assay on cerebrospinal fluid mononuclear cells
No full textCentral nervous system tuberculosis remains a clinical diagnostic challenge. The ex vivo Mycobacterium tuberculosis-specific enzyme-linked immunospot assay (ELISPOT) is a novel assay for the rapid detection of M. tuberculosis-specific T-lymphocytes in the peripheral blood. However, when performed on peripheral blood, this assay cannot distinguish between active tuberculosis or latent tuberculosis infection. On the assumption that M. tuberculosis-specific T-lymphocytes migrate to sites of infection, we were able to demonstrate high levels of M. tuberculosis-specific cells by ELISPOT in the cerebrospinal fluid of a patient with tuberculous meningitis and intracerebral tuberculoma four weeks before cerebrospinal fluid culture became positive for M. tuberculosis by culture
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