Publications
215 results found
Perraudeau M, Taylor PR, Stauss HJ, et al., 2000, Altered major histocompatibility complex class II peptide loading in H2-O-deficient mice, European Journal of Immunology, Vol: 30, Pages: 2871-2880, ISSN: 0014-2980
The biosynthesis of MHC class II/peptide complexes involves classical, cell surface MHC products as well as the intracellular component H2-M, required for the removal of invariant chain-derived CLIP and for peptide loading. The function of another intracellular class II heterodimer, H2-O, is the matter of some controversy. The physical association of H2-O with H2-M and co-localization in class II+ vesicles suggest a related function in peptide exchange. Furthermore, the distinctive thymic distribution of H2-O raises the possibility of a specialized role in T cell thymic selection. To investigate the role of H2-O in vivo we generated mice carrying a targeted disruption in the H2-Oa gene. No evidence was obtained for a defect in removal of CLIP. However, the array of endogenous peptides bound by class II was altered and a defect in antigen presentation through H2-A to T cells was seen on the 129/Sv/C57BL/6 mixed strain background but not in 129/Sv pure strain mice. Furthermore, H2-O-null mice showed enhanced selection of CD4+ single positive thymocytes. The findings indicate that H2-O interacts with H2-M in peptide editing but that the genetic background in which H2-O deficiency is manifest is also important. Overall, the experiments indicate that H2-O/HLA-DO should be regarded as neither up-regulating nor down-regulating the DM-dependent release of CLIP, but as a modulator of peptide editing, determining the presenting cell type specific peptide profile able to retain stability in the class II groove.
Perraudeau M, Taylor PR, Stauss HJ, et al., 2000, Altered major histocompatibility complex class II peptide loading in H2-O-deficient mice, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 30, Pages: 2871-2880, ISSN: 0014-2980
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- Citations: 42
Taylor PR, Carugati A, Fadok VA, et al., 2000, A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo, Journal of Experimental Medicine, Vol: 192, Pages: 359-366, ISSN: 1540-9538
The strongest susceptibility genes for the development of systemic lupus erythematosus (SLE) in humans are null mutants of classical pathway complement proteins. There is a hierarchy of disease susceptibility and severity according to the position of the missing protein in the activation pathway, with the severest disease associated with C1q deficiency. Here we demonstrate, using novel in vivo models of apoptotic cell clearance during sterile peritonitis, a similar hierarchical role for classical pathway complement proteins in vivo in the clearance of apoptotic cells by macrophages. Our results constitute the first demonstration of an impairment in the phagocytosis of apoptotic cells by macrophages in vivo in a mammalian system. Apoptotic cells are thought to be a major source of the autoantigens of SLE, and impairment of their removal by complement may explain the link between hereditary complement deficiency and the development of SLE.
Bygrave AE, Botto M, 2000, Knocking out complement genes., Methods Mol Biol, Vol: 150, Pages: 215-228, ISSN: 1064-3745
Norsworthy P, Theodoridis E, Botto M, et al., 1999, Overrepresentation of the Fcγ receptor type IIA R131/R131 genotype in Caucasoid systemic lupus erythematosus patients with autoantibodies to C1q and glomerulonephritis, ARTHRITIS AND RHEUMATISM, Vol: 42, Pages: 1828-1832, ISSN: 0004-3591
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- Citations: 74
Norsworthy PJ, Taylor PR, Walport MJ, et al., 1999, Cloning of the mouse homolog of the 126-kDa human C1q/MBL/SP-A receptor, C1qR<sub>p</sub>, MAMMALIAN GENOME, Vol: 10, Pages: 789-793, ISSN: 0938-8990
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- Citations: 18
Naughton MA, Battaglia E, O'Brien S, et al., 1999, Identification of thiopurine methyltransferase (TPMT) polymorphisms cannot predict myelosuppression in systemic lupus erythematosus patients taking azathioprine, RHEUMATOLOGY, Vol: 38, Pages: 640-644, ISSN: 1462-0324
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- Citations: 63
Bickerstaff MCM, Botto M, Hutchinson WL, et al., 1999, Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity, NATURE MEDICINE, Vol: 5, Pages: 694-697, ISSN: 1078-8956
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- Citations: 401
Robson MG, Cook HT, Botto M, et al., 1999, C1q deficient mice develop severe disease in accelerated nephrotoxic nephritis., KIDNEY INTERNATIONAL, Vol: 55, Pages: 2593-2593, ISSN: 0085-2538
Mitchell DA, Taylor PR, Cook HT, et al., 1999, Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation, JOURNAL OF IMMUNOLOGY, Vol: 162, Pages: 5676-5679, ISSN: 0022-1767
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- Citations: 75
Walport MJ, Davies KA, Botto M, 1998, Clq and systemic lupus erythematosus, IMMUNOBIOLOGY, Vol: 199, Pages: 265-285, ISSN: 0171-2985
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- Citations: 289
Cutler AJ, Botto M, van Essen D, et al., 1998, T cell-dependent immune response in C1q-deficient mice:: Defective interferon γ production by antigen-specific T cells, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 187, Pages: 1789-1797, ISSN: 0022-1007
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- Citations: 80
Botto M, Dell'Agnola C, Bygrave AE, et al., 1998, Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies, NATURE GENETICS, Vol: 19, Pages: 56-59, ISSN: 1061-4036
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- Citations: 1165
Taylor P, Botto M, Walport M, 1998, The complement system, CURRENT BIOLOGY, Vol: 8, Pages: R259-R261, ISSN: 0960-9822
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- Citations: 28
Robson MG, Cook HT, Botto M, et al., 1998, Delayed resolution of inflammation in heterologous nephrotoxic nephritis in Clq deficient mice, MOLECULAR IMMUNOLOGY, Vol: 35, Pages: 343-343, ISSN: 0161-5890
Taylor PR, Nash JT, Theodoridis E, et al., 1998, A targeted disruption of the murine complement factor B gene resulting in loss of expression of three genes in close proximity, factor B, <i>C2</i>, and <i>D17H6S45</i>, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 273, Pages: 1699-1704, ISSN: 0021-9258
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- Citations: 52
Botto M, 1998, C1q knock-out mice for the study of complement deficiency in autoimmune disease, EXPERIMENTAL AND CLINICAL IMMUNOGENETICS, Vol: 15, Pages: 231-234, ISSN: 0254-9670
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- Citations: 80
Taylor PR, Slingsby JH, Walport MJ, et al., 1997, Murine D17H6S45 (Rd) gene: polymorphism and overlap with complement factor B, MAMMALIAN GENOME, Vol: 8, Pages: 796-797, ISSN: 0938-8990
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- Citations: 1
Botto M, Hawkins PN, Bickerstaff MCM, et al., 1997, Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene, NATURE MEDICINE, Vol: 3, Pages: 855-859, ISSN: 1078-8956
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- Citations: 209
Walport MJ, Davies KA, Morley BJ, et al., 1997, Complement deficiency and autoimmunity, B LYMPHOCYTES AND AUTOIMMUNITY, Vol: 815, Pages: 267-281, ISSN: 0077-8923
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- Citations: 83
NasonBurchenal K, Gandini D, Botto M, et al., 1996, Interferon augments PML and PML/RAR alpha expression in normal myeloid and acute promyelocytic cells and cooperates with all-trans retinoic acid to induce maturation of a retinoid-resistant promyelocytic cell line, BLOOD, Vol: 88, Pages: 3926-3936, ISSN: 0006-4971
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- Citations: 56
Naughton MA, Walport MJ, Wurzner R, et al., 1996, Organ-specific contribution to circulating C7 levels by the bone marrow and liver in humans, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 26, Pages: 2108-2112, ISSN: 0014-2980
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- Citations: 24
Botto M, Theodoridis E, Thompson EM, et al., 1996, Fc gamma RIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease., Clin Exp Immunol, Vol: 104, Pages: 264-268, ISSN: 0009-9104
An allotypic variant of Fc gamma RIIa, Fc gamma RIIa-HR (Fc gamma RIIa-R131), has been shown in vitro to reduce the capacity of phagocytic cells to bind and internalize IgG-containing immune complexes. Our aim was to determine whether this allotypic variant was associated with susceptibility to SLE and the development of lupus nephritis, as previous studies have suggested. Fc gamma RIIA genotype analysis was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) in 215 Caucasoid, 70 Afro-Caribbean, and 46 Chinese patients with SLE, and in 259,77 and 49 ethnically matched controls, respectively. Distribution of Fc gamma RIIa genotypes between the patients and ethnically matched controls was not significantly different in the three populations studied. No association between the Fc gamma RIIa-HR allotype and nephritis was found. Our results suggest that the Fc gamma RIIa-HR allotype is not a major factor predisposing to the development of SLE, or to lupus nephritis.
Naughton MA, Botto M, Carter MJ, et al., 1996, Extrahepatic secreted complement C3 contributes to circulating C3 levels in humans, JOURNAL OF IMMUNOLOGY, Vol: 156, Pages: 3051-3056, ISSN: 0022-1767
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- Citations: 62
Petry F, McClive PJ, Botto M, et al., 1996, The mouse C1q genes are clustered on chromosome 4 and show conservation of gene organization, IMMUNOGENETICS, Vol: 43, Pages: 370-376, ISSN: 0093-7711
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- Citations: 12
HOHLER T, BOTTO M, RITTNER C, et al., 1995, COMPLEMENT COMPONENT C3 - MOLECULAR-BASIS OF THE C3-ASTERISK-S025 VARIANT AND EVIDENCE FOR MOLECULAR HETEROGENEITY OF OTHER VARIANTS, HUMAN GENETICS, Vol: 96, Pages: 539-541, ISSN: 0340-6717
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- Citations: 2
WALPORT MJ, DAVIES KA, BOTTO M, et al., 1994, C3 NEPHRITIC FACTOR AND SLE - REPORT OF 4 CASES AND REVIEW OF THE LITERATURE, QUARTERLY JOURNAL OF MEDICINE, Vol: 87, Pages: 609-615, ISSN: 0033-5622
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- Citations: 48
BOTTO M, LISSANDRINI D, SORIO C, et al., 1992, BIOSYNTHESIS AND SECRETION OF COMPLEMENT COMPONENT (C3) BY ACTIVATED HUMAN POLYMORPHONUCLEAR LEUKOCYTES, JOURNAL OF IMMUNOLOGY, Vol: 149, Pages: 1348-1355, ISSN: 0022-1767
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- Citations: 96
BOTTO M, FONG KY, SO AK, et al., 1992, HOMOZYGOUS HEREDITARY C3 DEFICIENCY DUE TO A PARTIAL GENE DELETION, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 89, Pages: 4957-4961, ISSN: 0027-8424
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- Citations: 50
BOTTO M, FONG KY, SO AK, et al., 1990, MOLECULAR-BASIS OF POLYMORPHISMS OF HUMAN-COMPLEMENT COMPONENT-C3, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 172, Pages: 1011-1017, ISSN: 0022-1007
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- Citations: 82
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