Table 2.
Overview of publications in the disease clusters autoimmunity and infectiology.
Disease entity | oc | Disease model | Gene manipulation and genetic background | Sex | Ref | |
---|---|---|---|---|---|---|
Immunology | ||||||
Autoimmunity | - | C1qKO induced SLE | 129/Ola, 129/Ola×C57BL/6 F2 | f/m | (9) | |
- | C1qKO induced SLE | 129/Sv, 129/Sv×C57BL/6 F2 | f/m | (64) | ||
- | C1qKO induced SLE | f/m | (65) | |||
- | C1qKO induced SLE | 129/Sv, 129/Sv×C57BL/6, C57BL/6 | f/m | (66) | ||
= | C1qKO induced SLE | C1qa-/- IgHEL, C1qa-/- IgHEL/sHEL | f/m | (67) | ||
- | C1qKO induced SLE | 129/Ola×C57BL/6 | f/m | (68) | ||
- | C1qKO induced SLE | 129/Sv×C57BL/6, C57BL/6 | f/m | (69) | ||
= | C1qKO induced SLE | f/m | (70) | |||
- | C1qKO induced SLE | C57BL/6.C1q-/- , C57BL/6.lpr/lpr.C1q-/ -, MRL/Mp-lpr/lpr.C1q-/- | f/m | (71) | ||
- | C1qKO induced SLE | MRL/Mp.C1q-/- , | f/m | (72) | ||
- | Cq1KO induced SLE | 129×B6 F2 | f | (73) | ||
- | Cq1KO induced SLE | C1q-/-IgHEL, C1q-/-IgHEL/mHEL-KK | f/m | (74) | ||
= | Cq1KO induced SLE | VH3H9R/VLκ8R.MRL/Mp.C1qa-/- , VH3H9R.MRL/Mp.C1qa-/- | f/m | (75) | ||
+ | pristane induced SLE | BALB/c | f | (76) | ||
- | Cq1KO induced SLE | f | (77) | |||
- | Cq1KO induced SLE | f | (78) | |||
- | autoimmunity | MRL/Mp.C1q-/- , C57BL/6.C1q-/- | f | (79) | ||
Autoimmune nephropathy | - | LN | C1qa-/- , C1qa/H2-Bf/C2-/- , 129/Sv×C57BL/6 | f/m | (80) | |
- | LN | Sle1.C1q-/-, Sle1.Mfge8-/-C1q-/- | f/m | (81) | ||
= | LN | m | (82) | |||
- | Anti-GBM GN | C1qa-/-, C1qa/H2-Bf/C2-/-, 129/Sv×C57BL/6 | f/m | (83) | ||
- | Anti-GBM GN | 129/Sv×C57BL/6, C57BL/6 | f/m | (84) | ||
= | Anti-GBM GN | f/m | (85) | |||
= | Cryoglobulinemic GN | BALB/c | f/m | (86) | ||
= | FSG sclerosis | BALB/c | f | (87) | ||
= | tubulointestinal fibrosis | m | (88) | |||
Transplant rejection | - | transplant at rejection | f | (89) | ||
- | transplant at rejection | C57BL/6, BALBc | f | (90) | ||
- | transplant at rejection | f | (91) | |||
Arthritis | = | arthritis | C1q-/- , C1q-/-/MBL-/- | f/m | (92) | |
+ | arthritis | C1q-/-/Df-/- | f/m | (93) | ||
= | anaphylaxis | 129/SV | f/m | (94) | ||
Vaccination | = | rhesus prophylaxe | f/m | (95) | ||
+ | immunoprophylaxis | (96) | ||||
= | HSV- Impfung | f | (97) | |||
= | adenoviral vectors | f/m | (98) | |||
= | adenoviral vectors | m | (99) | |||
- | IBD | C1q/MBL-/- | f/m | (100) | ||
+ | sterile inflammation | C1q-/-, C1q/fD-/- | f/m | (101) | ||
Infectiology | ||||||
Bacterial infections | - | S. Pneumoniae | f/m | (102) | ||
- | S. Pneumoniae | f/m | (103) | |||
- | S. Pneumoniae septicaemie | f/m | (104) | |||
- | S. Pneumoniae meningitis | f/m | (105) | |||
- | S. Pneumoniae acute otitis | f/m | (106) | |||
- | S. Pneumoniae acute otitis | f/m | (107) | |||
- | S. Pneumoniae acute otitis | f/m | (108) | |||
- | S. Pyogenes septicaemie | f/m | (109) | |||
- | polymicrobial peritonitis | 129/SV | m | (110) | ||
- | polymicrobial peritonitis | 129/SV | f/m | (111) | ||
- | polymicrobial peritonitis | f/m | (112) | |||
- | Salmonella enterica | 129/SV | m | (113) | ||
- | Borrelia burgdorferi | f/m | (114) | |||
- | Rickettsia australis | f/m | (115) | |||
New therapeutica | - | N. gonorrhoeae | f | (116) | ||
- | N. gonorrhoeae | f | (117) | |||
= | N. gonorrhoeae | f | (118) | |||
= | P. aeruginosa | m | (119) | |||
Other pathogens | - | West Nile virus | C1q-/-, C1q×fD-/- | f/m | (120) | |
- | Malaria | 129/Sv | f | (121) | ||
= | Nematode | – | f/m | (122) | ||
= | Cryptosporidium | – | f/m | (123) | ||
= | Candida albicans | – | f/m | (124) |
Each cluster is subdivided according to disease and organ manifestation, respectively. Disease outcome (oc) of C1qKO mice compared to wt and/or C1q sufficient mice in the investigated disease model is given as “+” respectively turquoise =beneficial, “-” respectively ocher =detrimental, “=“ respectively grey=no effect. The overall outcome on the disease entity is similarly color coded using lighter shades for ambiguous group results. Genetic modifications other than C1qKO and genetic background other than C57BL/6 are listed explicitly. In studies with several C1q deficient mice, all C1q deficient mice are listed. Sex as indicated in the study (f=female only, m=male only, f/m=mixed gender); if not mentioned explicitly by the study, mixed gender was assumed. FSG, focal segmental glomerulosclerosis; GBM, glomerular basement membrane; GN, Glomerulonephritis; HSV, herpes simplex virus; IBD, inflammatory bowel disease; LN, lupus nephritis; N., Neisseria; P., Pseudomonas aeruginosa; S., Streptococcus; SLE, systemic lupus erythematosus.