ProfessorMatthewPickering

Taylor SRJ, Turner CM, Elliott JI, McDaid J, Hewitt R, Smith J, Pickering MC, Whitehouse DL, Cook HT, Burnstock G, Pusey CD, Unwin RJ, Tam FWKet al., 2009, P2X₇ Deficiency Attenuates Renal Injury in Experimental Glomerulonephritis, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 20, Pages: 1275-1281, ISSN: 1046-6673

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• Citations: 98

Paixao-Cavalcante D, Hanson S, Botto M, Cook HT, Pickering MCet al., 2009, Factor H facilitates the clearance of GBM bound iC3b by controlling C3 activation in fluid phase, MOLECULAR IMMUNOLOGY, Vol: 46, Pages: 1942-1950, ISSN: 0161-5890

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• Citations: 35

Ruseva MM, Hughes TR, Donev RM, Sivasankar B, Pickering MC, Wu X, Harris CL, Morgan BPet al., 2009, Crry deficiency in complement sufficient mice: C3 consumption occurs without associated renal injury, MOLECULAR IMMUNOLOGY, Vol: 46, Pages: 803-811, ISSN: 0161-5890

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• Citations: 20

Paixao-Cavalcante D, Botto M, Cook HT, Pickering MCet al., 2009, Shiga toxin-2 results in renal tubular injury but not thrombotic microangiopathy in heterozygous factor H-deficient mice, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 155, Pages: 339-347, ISSN: 0009-9104

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• Citations: 19

Pickering MC, Macor P, Fish J, Durigutto P, Bossi F, Petry F, Botto M, Tedesco Fet al., 2008, Complement C1q and C8β deficiency in an individual with recurrent bacterial meningitis and adult-onset systemic lupus erythematosus-like illness, RHEUMATOLOGY, Vol: 47, Pages: 1588-1589, ISSN: 1462-0324

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• Citations: 13

Pickering MC, Cook HT, 2008, Translational Mini-Review Series on Complement Factor H: Renal diseases associated with complement factor H: novel insights from humans and animals, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 151, Pages: 210-230, ISSN: 0009-9104

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• Citations: 135

Rose KL, Paixao-Cavalcante D, Fish J, Manderson AP, Malik TH, Bygrave AE, Lin T, Sacks SH, Walport MJ, Cook HT, Botto M, Pickering MCet al., 2008, Factor I is required for the development of membranoproliferative glomerulonephritis in factor H-deficient mice, JOURNAL OF CLINICAL INVESTIGATION, Vol: 118, Pages: 608-618, ISSN: 0021-9738

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• Citations: 104

Coffey PJ, Gias C, McDermott CJ, Lundh P, Pickering MC, Sethi C, Bird A, Fitzke FW, Maass A, Chen LL, Holder GE, Luthert PJ, Salt TE, Moss SE, Greenwood Jet al., 2007, Complement factor H deficiency in aged mice causes retinal abnormalities and visual dysfunction, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 104, Pages: 16651-16656, ISSN: 0027-8424

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• Citations: 163

Smith RJH, Alexander J, Barlow PN, Botto M, Cassavant TL, Cook HT, de Cordoba SR, Hageman GS, Jokiranta TS, Kimberling WJ, Lambris JD, Lanning LD, Levidiotis V, Licht C, Lutz HU, Meri S, Pickering MC, Quigg RJ, Rops AL, Salant DJ, Sethi S, Thurman JM, Tully HF, Tully SP, van der Vlag J, Walker PD, Wuerzner R, Zipfel PFet al., 2007, New approaches to the treatment of dense deposit disease, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 18, Pages: 2447-2456, ISSN: 1046-6673

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• Citations: 179

Pickering MC, de Jorge EG, Martinez-Barricarte R, Recalde S, Garcia-Layana A, Rose KL, Moss J, Walport MJ, Cook HT, de Cordoba SR, Botto Met al., 2007, Spontaneous hemolytic uremic syndrome triggered by complement factor H lacking surface recognition domains, Journal of Experimental Medicine, Vol: 204, Pages: 1249-1256, ISSN: 0022-1007

Factor H (FH) is an abundant serum glycoprotein that regulates the alternative pathway of complement-preventing uncontrolled plasma C3 activation and nonspecific damage to host tissues. Age-related macular degeneration (AMD), atypical hemolytic uremic syndrome (aHUS), and membranoproliferative glomerulonephritis type II (MPGN2) are associated with polymorphisms or mutations in the FH gene (Cfh), suggesting the existence of a genotype–phenotype relationship. Although AMD and MPGN2 share pathological similarities with the accumulation of complement-containing debris within the eye and kidney, respectively, aHUS is characterized by renal endothelial injury. This pathological distinction was reflected in our Cfh association analysis, which demonstrated that although AMD and MPGN2 share a Cfh at-risk haplotype, the haplotype for aHUS was unique. FH-deficient mice have uncontrolled plasma C3 activation and spontaneously develop MPGN2 but not aHUS. We show that these mice, transgenically expressing a mouse FH protein functionally equivalent to aHUS-associated human FH mutants, regulate C3 activation in plasma and spontaneously develop aHUS but not MPGN2. These animals represent the first model of aHUS and provide in vivo evidence that effective plasma C3 regulation and the defective control of complement activation on renal endothelium are the critical events in the molecular pathogenesis of FH-associated aHUS.

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Abrera-Abeleda MA, Xu Y, Pickering MC, Smith RJH, Sethi Set al., 2007, Mesangial immune complex glomerulonephritis due to complement factor D deficiency, KIDNEY INTERNATIONAL, Vol: 71, Pages: 1142-1147, ISSN: 0085-2538

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• Citations: 19

Pickering MC, Warren J, Rose KL, Carlucci F, Wang Y, Walport MJ, Cook HT, Botto Met al., 2006, Prevention of C5 activation ameliorates spontaneous and experimental factor H-deficient glomerulonephritis in mice, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 103, Pages: 9649-9654, ISSN: 0027-8424

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• Citations: 117

Braun MC, Li L, Ke B, Dubinsky WP, Pickering MC, Chang J-Yet al., 2006, Proteomic profiling of urinary protein excretion in the factor H-deficient mouse, AMERICAN JOURNAL OF NEPHROLOGY, Vol: 26, Pages: 127-135, ISSN: 0250-8095

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• Citations: 13

Alexander JJ, Pickering MC, Haas M, Osawe I, Quigg RJet al., 2005, Complement factor H limits immune complex deposition and prevents inflammation and scarring in glomeruli of mice with chronic serum sickness, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 16, Pages: 52-57, ISSN: 1046-6673

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• Citations: 45

Patel SM, Cohen P, Pickering MC, Gazzard BG, Andreyev Jet al., 2003, Successful treatment of acute haemorrhagic cytomegalovirus colitis with ganciclovir in an individual without overt immunocompromise, EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY, Vol: 15, Pages: 1055-1060, ISSN: 0954-691X

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• Citations: 7

Pickering MC, Cook HT, Warren J, Bygrave AE, Moss J, Walport MJ, Botto Met al., 2002, Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H, NATURE GENETICS, Vol: 31, Pages: 424-428, ISSN: 1061-4036

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• Citations: 387

Taylor PR, Pickering MC, Kosco-Vilbois MH, Walport MJ, Botto M, Gordon S, Martinez-Pomares Let al., 2002, The follicular dendritic cell restricted epitope, FDC-M2, is complement C4; localization of immune complexes in mouse tissues, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 32, Pages: 1888-1896, ISSN: 0014-2980

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• Citations: 60

Mitchell DA, Pickering MC, Warren J, Fossati-Jimack L, Cortes-Hernandez J, Cook HT, Botto M, Walport MJet al., 2002, C1q deficiency and autoimmunity: The effects of genetic background on disease expression, JOURNAL OF IMMUNOLOGY, Vol: 168, Pages: 2538-2543, ISSN: 0022-1767

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• Citations: 179

Manderson AP, Pickering MC, Botto M, Walport MJ, Parish CRet al., 2001, Continual low-level activation of the classical complement pathway, Journal of Experimental Medicine, Vol: 194, Pages: 747-756, ISSN: 0022-1007

There is evidence that the classical complement pathway may be activated via a “C1-tickover” mechanism, analogous to the C3-tickover of the alternative pathway. We have quantitated and characterized this pathway of complement activation. Analysis of freshly collected mouse and human plasma revealed that spontaneous C3 activation rapidly occurred with the generation of C3 fragments in the plasma. By the use of complement- and Ig-deficient mice it was found that C1q, C4, C2, and plasma Ig were all required for this spontaneous C3 activation, with the alternative complement pathway further amplifying C3 fragment generation. Study of plasma from a human with C1q deficiency before and after therapeutic C1q infusion confirmed the existence of a similar pathway for complement activation in humans. Elevated levels of plasma C3 were detected in mice deficient in complement components required for activation of either the classical or alternative complement pathways, supporting the hypothesis that there is continuous complement activation and C3 consumption through both these pathways in vivo. Blood stasis was found to stimulate C3 activation by classical pathway tick-over. This antigen-independent mechanism for classical pathway activation may augment activation of the complement system at sites of inflammation and infarction.

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Pickering MC, Warren J, Bygrave AE, Moss J, Sim RB, Cook HT, Walport MJ, Botto Met al., 2001, Membranoproliferative glomerulonephritis in factor H-deficient mice, MOLECULAR IMMUNOLOGY, Vol: 38, Pages: 116-117, ISSN: 0161-5890

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Pickering MC, Fischer S, Lewis MR, Walport MJ, Botto M, Cook HTet al., 2001, Ultraviolet-radiation-induced keratinocyte apoptosis in C1q-deficient mice, JOURNAL OF INVESTIGATIVE DERMATOLOGY, Vol: 117, Pages: 52-58, ISSN: 0022-202X

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• Citations: 33

Pickering MC, Botto M, Taylor PR, Lachmann PJ, Walport MJet al., 2001, Systemic lupus erythematosus, complement deficiency, and apoptosis, ADVANCES IN IMMUNOLOGY, VOL. 76, Vol: 76, Pages: 227-324, ISSN: 0065-2776

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• Citations: 53

Pickering MC, Haskard DO, 2000, False-positive results obtained using the Mantoux test in Behcet's syndrome: comment on the article by Garcia-Porrua et al, ARTHRITIS AND RHEUMATISM, Vol: 43, Pages: 2855-2855, ISSN: 0004-3591

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• Citations: 3

Pickering MC, Haskard DO, 2000, Behcet's syndrome, JOURNAL OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON, Vol: 34, Pages: 169-177, ISSN: 0035-8819

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• Citations: 20

Pickering MC, Barkham T, Mason JC, Shaunak S, Davies KAet al., 2000, Bilateral gluteal abscesses as a unique manifestation of <i>Fusobacterium</i> septicaemia, RHEUMATOLOGY, Vol: 39, Pages: 224-225, ISSN: 1462-0324

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• Citations: 8

Pickering MC, Walport MJ, 2000, Links between complement abnormalities and systemic lupus erythematosus, RHEUMATOLOGY, Vol: 39, Pages: 133-141, ISSN: 1462-0324

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• Citations: 106

Pickering MC, Walport MJ, 1998, Eosinophilic myopathic syndromes., Curr Opin Rheumatol, Vol: 10, Pages: 504-510, ISSN: 1040-8711

Eosinophilic infiltration into skeletal muscle, although rare, has been described in a diverse group of conditions. It most commonly occurs in parasitic infection as focal eosinophilic myositis but can be a feature of systemic hypereosinophilic conditions such as eosinophilia-myalgia syndrome and idiopathic hypereosinophilic syndrome. The majority of cases have no discernible etiological factor. Eosinophilic myopathies should be distinguished from the commoner idiopathic inflammatory myopathies such as polymyositis and dermatomyositis. This report describes the various conditions in which eosinophilic myopathy occurs and reviews the current state of knowledge of eosinophilic myopathy.

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