Cold-dependent activation of complement: Recognition, assessment, and mechanism
dc.contributor.author | Zuraw, Bruce L. | en_US |
dc.contributor.author | Herschbach, Jack H. | en_US |
dc.contributor.author | Chambers, Sandra L. | en_US |
dc.contributor.author | Mathews, Kenneth P. | en_US |
dc.contributor.author | Mentyka, Robert A. | en_US |
dc.contributor.author | Hugli, Tony E. | en_US |
dc.date.accessioned | 2006-09-11T15:20:57Z | |
dc.date.available | 2006-09-11T15:20:57Z | |
dc.date.issued | 1992-09 | en_US |
dc.identifier.citation | Mathews, Kenneth P.; Mentyka, Robert A.; Chambers, Sandra L.; Hugli, Tony E.; Herschbach, Jack H.; Zuraw, Bruce L.; (1992). "Cold-dependent activation of complement: Recognition, assessment, and mechanism." Journal of Clinical Immunology 12(5): 362-370. <http://hdl.handle.net/2027.42/44843> | en_US |
dc.identifier.issn | 1573-2592 | en_US |
dc.identifier.issn | 0271-9142 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44843 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1430107&dopt=citation | en_US |
dc.description.abstract | Cold-dependent activation of complement (CDAC) is a phenomenon characterized by low hemolytic complement activity in chilled serum. Complement component levels are normal when measured immunologically, and there is normal hemolytic activity in EDTA plasma or serum maintained at 37°C. Little attention has been paid to CDAC except in Japan, and current unfamiliarity with it, even by clinical immunologists, can lead to confusion and unnecessary laboratory tests. A 66-year-old patient with a complex medical history is described whose complement tests showed abnormalities characteristic of CDAC. Evidence for classical complement pathway activation in the cold was obtained by CH 50 measurements, by hemolytic C4 determinations, by C4a, C3a, and C4d generation, and by quantitating complexes. A good correlation was observed among these parameters. Cryoprecipitates were absent. CDAC activity has persisted for over 5 years and is greater at 13 than at 4°C. Activation is ablated by heating at 56°C and restored by the addition of C1 to the heated serum. Adsorption by streptococcal protein G-Sepharose and precipitation by 2.5% polyethylene glycol support the hypothesis that CDAC is caused by aggregated IgG. The CDAC factor(s) also induces complement activation in normal serum but has not interfered with Raji cell or C1q binding tests or with FACS analysis. More limited studies of a second individual experiencing CDAC yielded similar results. | en_US |
dc.format.extent | 1109919 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers-Plenum Publishers; Plenum Publishing Corporation ; Springer Science+Business Media | en_US |
dc.subject.other | C1 Inhibitor | en_US |
dc.subject.other | Complement | en_US |
dc.subject.other | IgG | en_US |
dc.subject.other | Immunology | en_US |
dc.subject.other | Biomedicine | en_US |
dc.subject.other | Medical Microbiology | en_US |
dc.subject.other | Internal Medicine | en_US |
dc.subject.other | Infectious Diseases | en_US |
dc.subject.other | Cryoproteins | en_US |
dc.subject.other | Anaphylatoxins | en_US |
dc.title | Cold-dependent activation of complement: Recognition, assessment, and mechanism | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Microbiology and Immunology | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Division of Allergy, Department of Internal Medicine, University of Michigan, 48109, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Department of Molecular and Experimental Medicine, SRB-6, The Scripps Research Institute, 92037, La Jolla, California | en_US |
dc.contributor.affiliationother | Department of Molecular and Experimental Medicine, SRB-6, The Scripps Research Institute, 92037, La Jolla, California | en_US |
dc.contributor.affiliationother | Department of Immunology, The Scripps Research Institute, 92037, La Jolla, California | en_US |
dc.contributor.affiliationother | Department of Molecular and Experimental Medicine, SRB-6, The Scripps Research Institute, 92037, La Jolla, California | en_US |
dc.contributor.affiliationother | Department of Molecular and Experimental Medicine, SRB-6, The Scripps Research Institute, 92037, La Jolla, California | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 1430107 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44843/1/10875_2004_Article_BF00920794.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00920794 | en_US |
dc.identifier.source | Journal of Clinical Immunology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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