17:
107:(C3aR). The C3aR is similarly structurally homologous to C5aR, but contains an extracellular domain with more than 160 amino acids. Specific binding sites for interactions between C3a and C3aR are unknown, but it has been shown that sulfation of tyrosine 174, one of the amino acids in the extracellular domain, is required for C3a binding. It has also been demonstrated that the C3aR N terminus is not required for ligand binding.
268:. Unlike C5a desArg, this version of C3a has no proinflammatory activity. However, ASP functions as a hormone in the adipose tissue, moderating fatty acid migration to adipocytes and triacylglycerol synthesis. In addition, it has been shown that ASP downregulates the polyclonal immune response in the same way C3a does.
226:
molecule production. C3aR signaling along antigen-presenting cells' CD28 and CD40L pathways also plays a role in T cell proliferation and differentiation. C3aR has been shown to be necessary for TH1 cell generation and regulates TH1 IL-10 expression, while an absence of active C3aR on dendritic cells upregulates
608:
Anna
Stokowska, Markus Aswendt, Daniel Zucha, Stephanie Lohmann, Frederique Wieters, Javier Morán Suarez, Alison L. Atkins, YiXian Li, Maria Miteva, Julia Lewin, Dirk Wiedermann, Michael Diedenhofen, Åsa Torinsson Naluai, Pavel Abaffy, Lukas Valihrach, Mikael Kubista, Mathias Hoehn, Milos Pekny, and
90:
C3a is a strongly basic and highly cationic 77 residue protein with a molecular mass of approximately 10 kDa. Residues 17-66 are made up of three anti-parallel helices and three disulfide bonds, which confer stability to the protein. The N-terminus consists of a fourth flexible helical structure,
212:
The roles of C3a in innate immunity, upon binding C3aR, include increased vasodilation via endothelial cell contraction, increased vascular permeability, and mast cell and basophil degranulation of histamine, induction of respiratory burst and subsequent degradation of pathogens by neutrophils,
243:
Levels of complement are regulated by moderating convertase formation and enzymatic activity. C3 convertase formation is primarily regulated by levels of active C3b and C4b. Factor I, a serine protease activated by cofactors, can cleave and C3b and C4b, thus preventing convertase formation. C3
225:
C3a also plays an important role in adaptive immunity, moderating leukocyte production and proliferation. C3a is able to regulate B cell and monocyte production of IL-6 and TNF-α, and human C3a has been shown to dampen the polyclonal immune response through dose-dependent regulation of B cell
216:
Traditionally thought to serve a strictly pro-inflammatory role, recent investigations have shown that C3a can also work against C5a to serve an anti-inflammatory role. In addition, migration and degranulation of neutrophils can be suppressed in the presence of C3a.
155:
on the antigen, including sugars. These bound receptors then complex with
Mannose-Binding Lectin-Associated Serine Proteases (MASPs), which have proteolytic activity similar to the C1 complex. The MASPs cleave C4 and C2, resulting in C3 convertase formation.
46:
C3a molecules induce responses through the GPCR C3a receptor. Like other anaphylatoxins, C3a is regulated by cleavage of its carboxy-terminal arginine, which results in a molecule with lowered inflammatory function (C3a desarginine).
213:
macrophages, and eosinophils, and regulation of cationic eosinophil protein migration, adhesion, and production. C3a is also able to play a role in chemotaxis for mast cells and eosinophils, but C5a is a more potent chemoattractant.
450:
Reid, Robert C.; Yau, Mei-Kwan; Singh, Ranee; Hamidon, Johan K.; Reed, Anthony N.; Chu, Peifei; Suen, Jacky Y.; Stoermer, Martin J.; Blakeney, Jade S.; Lim, Junxian; Faber, Jonathan M.; Fairlie, David P. (21 November 2013).
864:
Arlaud, G. J.; Gaboriaud, C.; Thielens, N. M.; Rossi, V.; Bersch, B.; Hernandez, J. F.; Fontecilla-Camps, J. C. (2001-04-01). "Structural biology of C1: dissection of a complex molecular machinery".
143:
mediates the classical pathway by activating the C1 complex, which cleaves C4 and C2 into smaller fragments (C4a, C4b, C2a, and C2b). C4a and C2b form C4bC2b, also known as C3 convertase.
77:
Initial research in mice demonstrating an effective treatment after stroke is leading to further investigation to determine whether application to humans has potential.
127:, which is involved in antigen opsonization. Other than the alternative pathway, which is constantly active, C3a formation is triggered by pathogenic infection.
168:
is typically always active at low levels in blood plasma through a process called tick-over, in which C3 spontaneously hydrolyzes into its active form, C3(H
70:
activation. It has been shown to have both proinflammatory and anti-inflammatory responses, its activity able to counteract the proinflammatory effects of
1237:
Barbu, Andreea; Hamad, Osama A.; Lind, Lars; Ekdahl, Kristina N.; Nilsson, Bo (2015-09-01). "The role of complement factor C3 in lipid metabolism".
196:
Anaphylatoxins are small complement peptides that induce proinflammatory responses in tissues. C3a is primarily regarded for its role in the
1325:
1085:. 12th European Meeting on Complement in Human Disease12th European Meeting on CHD12th European Meeting on Complement in Human Disease.
151:
The lectin pathway is activated when pattern-recognition receptors, like mannan-binding lectin or ficolins, recognize and bind to
717:
Ames, R. S.; Li, Y.; Sarau, H. M.; Nuthulaganti, P.; Foley, J. J.; Ellis, C.; Zeng, Z.; Su, K.; Jurewicz, A. J. (1996-08-23).
152:
612:
Complement C3a treatment accelerates recovery after stroke via modulation of astrocyte reactivity and cortical connectivity
670:"Denaturation and unfolding of human anaphylatoxin C3a: An unusually low covalent stability of its native disulfide bonds"
352:"Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells"
350:
Strainic, MG; Liu, J; Huang, D; An, F; Lalli, PN; Muqim, N; Shapiro, VS; Dubyak, GR; Heeger, PS; Medof, ME (March 2008).
184:
O)Bb, or fluid-phase C3-convertase. This complex has the ability to catalyze the formation of C3a and C3b after it binds
1539:
1178:
Merle, Nicolas S.; Noe, Remi; Halbwachs-Mecarelli, Lise; Fremeaux-Bacchi, Veronique; Roumenina, Lubka T. (2015-05-26).
1128:"C3a and C5a Are Chemotactic Factors for Human Mesenchymal Stem Cells, Which Cause Prolonged ERK1/2 Phosphorylation"
91:
while the C terminus is disordered. C3a has a regulatory process and a structure homologous to complement component
1077:
Klos, Andreas; Tenner, Andrea J.; Johswich, Kay-Ole; Ager, Rahasson R.; Reis, Edimara S.; Köhl, Jörg (2009-09-01).
815:
Crass, T.; Ames, R. S.; Sarau, H. M.; Tornetta, M. A.; Foley, J. J.; Köhl, J.; Klos, A.; Bautsch, W. (1999-03-26).
139:, made up of C1r and C1s serine proteases, recognizes the Fc region of IgM or IgG antibodies bound to a pathogen.
1318:
1358:
165:
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Gao, Jinming; Choe, Hyeryun; Bota, Dalena; Wright, Paulette L.; Gerard, Craig; Gerard, Norma P. (2003-09-26).
570:"Is the complement activation product C3a a proinflammatory molecule? Re-evaluating the evidence and the myth"
265:
1348:
668:
Chang, Jui-Yoa; Lin, Curtis C. -J.; Salamanca, Silvia; Pangburn, Michael K.; Wetsel, Rick A. (2008-12-15).
1018:
Merle, Nicolas S.; Church, Sarah
Elizabeth; Fremeaux-Bacchi, Veronique; Roumenina, Lubka T. (2015-01-01).
264:, a protease, cleaves the arginine residue from C3a, forming the desArg derivative of C3a, also known as
1740:
1311:
245:
40:
292:"Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg"
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249:
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Schraufstatter, Ingrid U.; DiScipio, Richard G.; Zhao, Ming; Khaldoyanidi, Sophia K. (2009-03-15).
768:"Sulfation of tyrosine 174 in the human C3a receptor is essential for binding of C3a anaphylatoxin"
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production. The absence of C3 has also been shown to decrease IL-2 receptor expression on T cells.
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453:"Downsizing a human inflammatory protein to a small molecule with equal potency and functionality"
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O) that allows it to bind to a plasma protein called Factor B. This complex is then cleaved by
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C3a induces an immunological response through a 482 residue G-protein-coupled receptor called
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123:. There are three pathways of activation, each of which leads to the formation of C3a and
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401:"Complement and macrophage crosstalk during process of angiogenesis in tumor progression"
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that function to speed up C3 convertase half-lives and avert convertase formation.
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O). This activation induces a conformational change in the thioester domain of C3(H
625:
Zhou, Wuding (2012-02-01). "The new face of anaphylatoxins in immune regulation".
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719:"Molecular cloning and characterization of the human anaphylatoxin C3a receptor"
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Bajic, Goran; Yatime, Laure; Klos, Andreas; Andersen, Gregers Rom (2013-02-01).
50:
C3a is an effector of the complement system with a range of functions including
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as an anaphylatoxin, moderating and activating multiple inflammatory pathways.
1241:. 15th European Meeting on Complement in Human Disease 2015, Uppsala, Sweden.
1020:"Complement System Part I - Molecular Mechanisms of Activation and Regulation"
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971:"New perspectives on mannan-binding lectin-mediated complement activation"
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C3a, like other anaphylatoxins, has a C-terminal arginine residue. Serum
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convertase activity is also regulated without C3b inactivation, through
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817:"Chimeric receptors of the human C3a receptor and C5a receptor (CD88)"
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The classical pathway of complement activation is initiated when the
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Dinasarapu, A R; Chandrasekhar, A; Sahu, A; Subramaniam, S (2012).
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Degn, Søren E.; Thiel, Steffen; Jensenius, Jens C. (2007-01-01).
922:"Complement and its role in innate and adaptive immune responses"
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C3a formation occurs through activation and cleavage of
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1079:"The role of the anaphylatoxins in health and disease"
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Clinical
Journal of the American Society of Nephrology
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Dunkelberger, Jason R.; Song, Wen-Chao (2010-01-01).
95:, with which it shares 36% of its sequence identity.
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615:, Journal of Clinical Investigation, March 30, 2023
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399:Khan, MA; Assiri, AM; Broering, DC (22 July 2015).
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518:"Molecules Great and Small: The Complement System"
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20:The classical and alternative complement pathways.
1299:http://www.merck.com/mmpe/sec13/ch163/ch163d.html
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39:that binds to the C3a receptor (C3aR), a class A
27:is one of the proteins formed by the cleavage of
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43:. It plays a large role in the immune response.
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1180:"Complement System Part II: Role in Immunity"
568:Coulthard, LG; Woodruff, TM (15 April 2015).
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516:Mathern, DR; Heeger, PS (4 September 2015).
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239:Regulation of complement activation
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1273:"Complement C3 (Human)"
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1024:Frontiers in Immunology
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208:Role in innate immunity
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117:complement component 3
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35:. C3a is a 77 residue
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1105:
1100:
1096:
1092:
1088:
1084:
1080:
1073:
1065:
1061:
1056:
1051:
1047:
1043:
1038:
1033:
1029:
1025:
1021:
1014:
1006:
1002:
998:
994:
989:
984:
980:
976:
975:Immunobiology
972:
965:
957:
953:
949:
945:
940:
935:
931:
927:
926:Cell Research
923:
916:
914:
912:
903:
899:
895:
891:
887:
883:
879:
875:
871:
867:
860:
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848:
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826:
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664:
656:
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648:
644:
640:
636:
632:
628:
627:Immunobiology
621:
614:
613:
605:
597:
593:
588:
583:
580:(8): 3542–8.
579:
575:
571:
564:
562:
553:
549:
544:
539:
535:
531:
527:
523:
519:
512:
504:
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429:
424:
419:
414:
410:
406:
402:
395:
387:
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378:
373:
369:
365:
362:(3): 425–35.
361:
357:
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346:
344:
335:
331:
326:
321:
317:
313:
309:
305:
301:
297:
293:
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205:
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199:
189:
187:
179:
167:
157:
154:
144:
142:
138:
128:
126:
122:
121:C3-convertase
118:
108:
106:
96:
94:
78:
75:
73:
69:
65:
61:
58:stimulation,
57:
53:
48:
44:
42:
38:
37:anaphylatoxin
34:
30:
26:
18:
1720:Opsonization
1715:inflammation
1703:Cytotoxicity
1620:
1610:
1590:C1-inhibitor
1586:
1483:
1449:
1430:
1381:
1276:
1242:
1238:
1232:
1187:
1183:
1135:
1131:
1121:
1086:
1082:
1072:
1027:
1023:
1013:
978:
974:
964:
932:(1): 34–50.
929:
925:
869:
865:
859:
824:
820:
810:
775:
771:
761:
726:
722:
712:
677:
673:
663:
630:
626:
620:
610:
604:
577:
573:
525:
521:
511:
460:
456:
445:
408:
404:
394:
359:
355:
299:
295:
259:
256:Deactivation
248:, including
242:
224:
215:
211:
195:
163:
150:
134:
114:
105:C3a receptor
102:
89:
76:
56:angiogenesis
49:
45:
24:
23:
872:: 136–145.
463:(1): 2802.
1580:Inhibitors
272:References
234:Regulation
137:C1 complex
68:macrophage
60:chemotaxis
1713:Inducing
1206:1664-3224
1154:0022-1767
1046:1664-3224
997:0171-2985
948:1748-7838
886:0105-2896
843:0021-9258
794:0021-9258
745:0021-9258
647:1878-3279
487:2041-1723
411:(1): 58.
316:1469-896X
192:Functions
186:properdin
111:Formation
81:Structure
64:mast cell
1735:Category
1705:(by MAC)
1696:Function
1624:Factor H
1604:Factor I
1458:Factor D
1453:Factor B
1342:Pathways
1259:25746915
1224:26074922
1162:19265162
1113:19477527
1064:26082779
1005:17544815
956:20010915
902:21136630
894:11414355
851:10085065
802:12871936
704:18854167
655:21856033
596:25848071
552:25568220
495:24257095
437:26198107
386:18328742
356:Immunity
334:23184394
178:Factor D
99:Receptor
1215:4443744
1190:: 257.
1104:2725201
1055:4451739
1030:: 262.
753:8702752
695:2636726
543:4559511
503:5465825
465:Bibcode
428:4511526
377:2646383
325:3588916
1472:Middle
1257:
1222:
1212:
1204:
1160:
1152:
1111:
1101:
1062:
1052:
1044:
1003:
995:
954:
946:
900:
892:
884:
849:
841:
800:
792:
751:
743:
702:
692:
653:
645:
594:
550:
540:
501:
493:
485:
435:
425:
384:
374:
332:
322:
314:
198:innate
52:T cell
1666:CD11c
1662:CD11b
1438:MASP2
1434:MASP1
1375:Early
1279:(2).
898:S2CID
499:S2CID
1670:CD18
1614:C4BP
1599:CD59
1587:CLA:
1533:Late
1493:iC3b
1255:PMID
1220:PMID
1202:ISSN
1158:PMID
1150:ISSN
1109:PMID
1060:PMID
1042:ISSN
1001:PMID
993:ISSN
952:PMID
944:ISSN
890:PMID
882:ISSN
847:PMID
839:ISSN
798:PMID
790:ISSN
749:PMID
741:ISSN
700:PMID
651:PMID
643:ISSN
592:PMID
548:PMID
491:PMID
483:ISSN
433:PMID
382:PMID
330:PMID
312:ISSN
200:and
164:The
1685:C5a
1680:C3a
1657:CR4
1652:CR3
1647:CR2
1642:CR1
1611:CL:
1545:C5b
1540:MAC
1510:C5b
1505:C5a
1489:C3b
1484:C3a
1443:MBL
1417:C4b
1412:C4a
1400:C1s
1395:C1r
1390:C1q
1281:doi
1247:doi
1210:PMC
1192:doi
1140:doi
1136:182
1099:PMC
1091:doi
1050:PMC
1032:doi
983:doi
979:212
934:doi
874:doi
870:180
829:doi
825:274
780:doi
776:278
731:doi
727:271
690:PMC
682:doi
678:480
635:doi
631:217
582:doi
578:194
538:PMC
530:doi
473:doi
423:PMC
413:doi
372:PMC
364:doi
320:PMC
304:doi
141:C1q
125:C3b
93:C5a
86:C3a
72:C5a
33:C3b
25:C3a
1737::
1621:A:
1565:C9
1560:C8
1555:C7
1550:C6
1500:C5
1479:C3
1450:A:
1431:L:
1424:C2
1407:C4
1385:C1
1382:C:
1275:.
1253:.
1243:67
1218:.
1208:.
1200:.
1186:.
1182:.
1170:^
1156:.
1148:.
1134:.
1130:.
1107:.
1097:.
1087:46
1081:.
1058:.
1048:.
1040:.
1026:.
1022:.
999:.
991:.
977:.
973:.
950:.
942:.
930:20
928:.
924:.
910:^
896:.
888:.
880:.
868:.
845:.
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823:.
819:.
796:.
788:.
774:.
770:.
747:.
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725:.
721:.
698:.
688:.
676:.
672:.
649:.
641:.
629:.
590:.
576:.
572:.
560:^
546:.
536:.
526:10
524:.
520:.
497:.
489:.
481:.
471:.
459:.
455:.
431:.
421:.
409:22
407:.
403:.
380:.
370:.
360:28
358:.
354:.
342:^
328:.
318:.
310:.
300:22
298:.
294:.
280:^
74:.
62:,
1668:/
1664:/
1597:/
1491:/
1436:/
1359:A
1354:L
1349:C
1327:e
1320:t
1313:v
1287:.
1283::
1261:.
1249::
1226:.
1194::
1188:6
1164:.
1142::
1115:.
1093::
1066:.
1034::
1028:6
1007:.
985::
958:.
936::
904:.
876::
853:.
831::
804:.
782::
755:.
733::
706:.
684::
657:.
637::
598:.
584::
554:.
532::
505:.
475::
467::
461:4
439:.
415::
388:.
366::
336:.
306::
182:2
174:2
170:2
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