Table 1.

Evidence of antibody-mediated protection against Mycobacterium tuberculosis infection

Criterion	Evidence	References
Passive Ab transfer studies	Eight independent groups have shown protection and/or modification of the course of mycobacterial infection in mice with passive transfer of mAbs to mycobacterial antigens (Table 2). Three independent groups have recently shown protection in mice with passive transfer of immune polyclonal sera.	Teitelbaum et al. 1998; Pethe et al. 2001; Chambers et al. 2004; Hamasur et al. 2004; Williams et al. 2004; Buccheri et al. 2009; Lopez et al. 2009; Balu et al. 2011 Roy et al. 2005; Guirado et al. 2006; Olivares et al. 2006
High Ab titer associated with reduced susceptibility	AM-containing conjugate vaccine elicits Ab response that reduces susceptibility to infection. BCG as well as Mtb antigen-containing conjugate and DNA/RNA vaccines elicit cellular and humoral immune responses and improve outcome of infection.	Hamasur et al. 2003; Glatman-Freedman et al. 2004 Huygen et al. 1996; Hamasur et al. 2003; Glatman-Freedman et al. 2004; Xue et al. 2004; de Valliere et al. 2005; Giri et al. 2006; Grover et al. 2006; Teixeira et al. 2006; Chang-hong et al. 2008; Kohama et al. 2008; Palma et al. 2008; Niu et al. 2011
Increased susceptibility in hosts with Ab deficits	Peak of childhood TB is temporally correlated with nadir in maternal Ab. Lack of Abs against certain mycobacterial antigens is associated with TB dissemination in children and adults. Lack of early humoral immune response in Mtb-infected nonhuman primates predicts high likelihood for reactivation disease. B-cell-deficient mice are more susceptible to TB. Polymeric IgR-deficient mice loose mycobacterial antigen-specific IgA response in saliva and are more susceptible to respiratory BCG infection. IgA deficiency increases susceptibility to mycobacterial infection in mice.	Beyazova et al. 1995; Cruz and Starke 2007; Donald et al. 2010 Sada et al. 1990; Costello et al. 1992; Boggian et al. 1996; Gupta et al. 1997; Dayal et al. 2008 Kunnath-Velayudhan et al. 2012 Vordermeier et al. 1996; Maglione et al. 2007, 2008 Tjarnlund et al. 2006 Rodriguez et al. 2005; Buccheri et al. 2007
Other	Existence of mycobactericidal Abs FcR-mediated phagocytosis promotes phagolysosomal fusion. FcR-mediated phagocytosis increases macrophage Ca2+ signaling and intracellular killing. Higher FcyRIA expression in (i) subjects with TB compared with LTBI, and (ii) subjects before compared with after antituberculous treatment. IgG bound to BCG enhances oxygen release in phagosomes and antimycobacterial activity of alveolar macrophages.	Conti et al. 1998 Armstrong and Hart 1975 Malik et al. 2000 Sutherland et al. 2013; Cliff et al. 2013 Suga et al. 1996

Data in table modified with permission from Achkar and Casadevall 2013.

mAb, monoclonal Ab; AM, arabinomannan; BCG, Bacillus Calmette–Guérin; Mtb, M. tuberculosis; TB, tuberculosis; FcR, Fc receptor; LTBI, latent Mtb infection.