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They are referred to as <jats:italic>B cell superantigens<\/jats:italic> (SAgs) and include protein A of <jats:italic>Staphylococcus aureus (S. aureus)<\/jats:italic>, gp120 of HIV\u20101, and protein L of <jats:italic>Peptostreptococcus magnus (P. magnus)<\/jats:italic>. In contrast to conventional antigens, B cell superantigens interact with conserved framework regions of immunoglobulins and can target a large proportion of B cells. In experimental models, they have been demonstrated to deplete B cell subsets responsible for innate functions, namely B\u20101a and marginal zone (MZ) B cells. As a result, the interactions of these superantigens with host cells impair the humoral immune response. In addition to providing clues toward understanding host\u2013pathogen interactions and microbial pathogenesis, B cell superantigens represent potential therapeutic agents that could be used to specifically modulate expansion of B cell subsets in diseased subjects. In systemic autoimmune diseases, for example, there is activation and expansion of B cells that secrete pathogenic autoantibodies. Their depletion results in clinical improvement in both experimental animals and patients. Currently, attempts are being made to specifically deplete pathogenic autoantibody\u2010producing B cells. Since B\u20101a and MZ B cells have been found to be expanded in autoimmune disorders, B cell superantigens, used alone or in combination with other biological agents, may have beneficial effects in autoimmune disease management.<\/jats:bold> <\/jats:p>","DOI":"10.1196\/annals.1397.038","type":"journal-article","created":{"date-parts":[[2007,4,2]],"date-time":"2007-04-02T21:06:52Z","timestamp":1175548012000},"page":"342-354","source":"Crossref","is-referenced-by-count":5,"title":["Exploitation of Host Signaling Pathways by B Cell Superantigens\u2014Potential Strategies for Developing Targeted Therapies in Systemic Autoimmunity"],"prefix":"10.1111","volume":"1095","author":[{"given":"MONCEF","family":"ZOUALI","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,3,19]]},"reference":[{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gene.6363941"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2185544"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2143(96)90161-4"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1948066"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(92)90277-A"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118915"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V91.2.585"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1089\/088922200309304"},{"key":"e_1_2_8_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/358255a0"},{"key":"e_1_2_8_11_2","doi-asserted-by":"crossref","first-page":"3091","DOI":"10.4049\/jimmunol.142.9.3091","article-title":"HIV\u20101 GP120\u2010mediated immune suppression and lymphocyte destruction in the absence of viral infection","volume":"142","author":"Weinhold K.J.","year":"1989","journal-title":"J. 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