Table 1.

Lymphoid cells respond to HMGB1.

	NK cells	B-cells	T-cells
Nuclear	Modulation of transcriptional activity of various genes, including steroid hormone receptors, NF-κB, p53/p73 transcriptional complexes, and some homeobox-containing protein (Erlandsson Harris and Andersson, 2004; Lotze and Tracey, 2005)
		Nuclear assistance in assembly of recombination activating gene 1/2(RAG1/2)-DNA complex for V(D)J recombination of B-cell receptors (BCR) and T-cell receptors (TCR) (Agrawal and Schatz, 1997; Dai et al., 2005)
Cytosolic	Regulation of autophagy (Tang et al., 2010a) (other cell types, not discovered in lymphoid cells yet)
		Recruitment of MyD88 to TLR-9 (Ivanov et al., 2007)
	Universal biosensor of nucleic acid (Yanai et al., 2012)
Extracellular	Synergy with other cytokines to modulate cell functions via binding cytokine receptors (CXCR4 for example)
	Increased IFN-γ secretion in macrophage-stimulated NK cells (DeMarco et al., 2005)	Activation and proliferation in the form of immune complex (HMGB1 + DNA) (Tian et al., 2007; Avalos et al., 2010)	Expansion, activation, and polarization of Th1 cells (Messmer et al., 2004; Dumitriu and Baruah, 2005; Sundberg et al., 2009)
		Spontaneous IL-8 production (McDonnell et al., 2011)	Infiltration of T-cells expressing lymphotoxin and tumor progression (He et al., 2012a)