Table 1. Impact of TRAF deficiency on T lymphocyte development and function.

Listed observations were published in one or more report, referenced here, and are organized by TRAF molecule and mouse model.

TRAF	Mouse model	Observations	References
1	TRAF1.Tg	• Normal TCR-mediated proliferation and CTL responses in vitro • Decreased TCR-mediated apoptosis and peptide-induced tolerance	9
	TRAF1−/−	• Viable mice with normal lymphocyte development • Increased TCR/CD28-mediated proliferation • Enhanced TCR/TNF-mediated phosphorylation of IκBα and JNK, and increased AP-1 activation • Decreased influenza-specific CD8 T cells due to increased Bim-mediated apoptosis • Decreased TCR/4–1BB-mediated NF-κB1 activation in CD8 T cells • Impaired resident memory CD8 T cell formation following influenza infection • Enhanced NF-κB2 activation	10, 14, 17
2	TRAF2−/−	• Early lethality due to runting and inflammation • Increased sensitivity of thymocytes to TNFR1-mediated cell death	23
	TRAF2−/−TNFα−/−	• Improved survival compared to Traf2−/− mice • Elevated serum cytokines leading to progressive inflammatory disease	23–25
	TRAF2.DN	• Viable mice with normal numbers of T cells • Hyperresponsive to CD3-mediated proliferation in the absence of costimulation • Decreased TCR/CD28-mediated proliferation • Decreased cytokine production upon 4–1BB or OX40 stimulation • Impaired memory T cell development	19, 20, 22
	LckCre-TRAF2fl/fl	• Normal numbers of total splenic CD4 T cells • Altered helper T cell differentiation (increased Th2 and Tregs, decreased Th17) • 50% reduction in total splenic CD8 T cells; 70% reduction in Tcm CD8 T cells • Impaired response of CD8 T cells to IL-15 signaling, restored by exogenous IL-15 • Constitutive NF-κB2 activation	27
3	TRAF3−/−	• Early lethality due to runting and inflammation • Defective T cell proliferation • Defective Ab response to T-dependent Ag	32
	LckCre-TRAF3fl/fl	• Normal T cell survival • Increased thymic Tregs • Constitutive NF-κB2 activation	26
	CD4Cre-TRAF3fl/fl	• Normal numbers of total CD4 and CD8 T cells • Increased IL-2-mediated thymic Treg maturation • Increased frequency of effector/memory CD4 T cells, and reduced naïve CD4 T cells • Impaired IL-15-mediated homeostatic survival and activation of central memory CD8 T cells • Decreased iNKT cells due to defective IL-15 signaling • Defective TCR/CD28 signaling, impacting proliferation and cytokine production • Enhanced IL-2R signaling • Constitutive NF-κB2 activation • Failure to clear L. monocytogenes infection • Defective Ab responses to T-dependent Ag	34, 35, 37, 38
	FoxP3Cre-TRAF3−/−	• Normal Treg frequencies • Impaired Treg function in vivo • Increased frequency of effector/memory CD4 T cells and production of high affinity Abs	36
5	TRAF5−/−(F1 hybrid from C57BL/6J x 129/J cross)	• Normal numbers of CD4 and CD8 T cells • Reduced CD27-mediated proliferation in response to signals through CD3 and costimulation	41
	TRAF5−/− (C57BL/6)	• Defective response to L. monocytogenes infection, mainly affecting memory CD8 T cells • Failure of CD27-mediated signaling to rescue CD8 T cells from apoptosis • Increased OX40-mediated Th2 cell differentiation and cytokine production • Enhanced IL-6R signaling • Enhanced IL-6-mediated Th17 differentiation • Decreased GITR-mediated NF-κB1, p38, and ERK activation • Decreased GITR-mediated IL-2 production	42, 43, 44, 46, 47
6	TRAF6−/−	• Early lethality due to runting and skeletal abnormalities • Th2-like inflammatory phenotype • Normal proportions of CD4 and CD8 T cells, with skewing of CD4s toward an activated phenotype • Enhanced TCR-mediated proliferation	51, 55
	CD4Cre-TRAF6fl/fl	• Enhanced TCR-mediated proliferation and resistance to anergy • Hyperactivation of PI3K and AKT • Increased Th17 differentiation • Defective thymic Treg development	56, 57, 59–62
	FoxP3Cre-TRAF6fl/fl	• Th2-like inflammatory phenotype • Impaired Treg proliferation • Increased conversion of FoxP3+ cells to to FoxP3- cells • Enhanced IL-2R signaling	60, 61