Table 1.

Immunological characteristics of poly(ADP-ribose)-polymerase-deficient mice

Knock down gene	General features	Cytokine/immunoglobulin production	T-cell and B-cell compartments
PARP-1	Knockout mice resistant to: Lipopolysaccharide-induced septic shock Streptozotomycin-induced diabetes Peroxynitrite-induced arthritis Oxazolone-induced contact hypersensitivity Reduced airway inflammation	↓ NF-κB, NF-AT and AP-1 activation ↓ IL-1β and TNF-α production ↓ iNOS expression ↓ selectins, integrins and ICAMs expression ↓ IL-2 production ↓ Th2 cytokines (IL-4/IL-5/IL-13) production ↓ T-cell proliferation ↑/= IFN-γ production = IL-17 production ↑ Xcl1, Ccl4 and Ccl9 expression ↓ Immunoglobulin gene conversion ↓ IgG2a ↑ IgA ↑ IgG2b	Cell number in lymphatic organs: Normal/small increase in T-cell number, CD4, CD8 cells; Normal B-cell number; Increased Foxp3+ Treg cell number
PARP-2	Genetic deletion or silencing provides protection in: Cerebral ischaemia Colitis Doxorubicin-induced vascular smooth muscle damage Impaired astrocyte activation	↓ IL-1β production ↓ TNF-α production ↓ iNOS expression	Altered thymopoiesis: Reduced thymus size Increased Noxa expression and apoptosis in DP thymocytes Reduced TCR expression and skewed TCR-α chain repertoire
PARP-14	Reduced airway inflammation	↓ Th2 cell responses and IgE production ↓ IgA production in antigen-specific response ↓ IL-4-induced B-cell survival	Normal overall cell numbers in thymus, spleen, and lymph nodes Fewer marginal zone B cells More follicular B cells

AP-1, activator protein 1; DP, double positive (CD4⁺ CD8⁺); Foxp3, forkhead box P3; ICAM, intercellular cell adhesion molecule; Ig, immunoglobulin; IL, interleukin; iNOS, inducible nitric oxide synthase; KO, knock out; LPS, lipopolysaccharide; PARP, poly(ADP-ribose)-polymerase; NF-AT, nuclear factor of activated T cells; NF-κB, nuclear factor-κB; Noxa, Latin for damage; TCR, antigen-specific T cell receptor; TNF, tumour necrosis factor; ↓, inhibition; ↑, upregulation.