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Here, we found that <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> cells are deficient in their ability to optimally stimulate CD4<jats:sup>+<\/jats:sup> T cells via the HLA class II pathway. This defect in CD4<jats:sup>+<\/jats:sup> T\u2010cell recognition was not associated with low levels of co\u2010stimulatory molecules on <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> cells, as addition of external co\u2010stimulation failed to elicit CD4<jats:sup>+<\/jats:sup> T\u2010cell activation by <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>. Further, the defect was not caused by faulty antigen\/class II interaction, because antigenic peptides bound with measurable affinity to <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\u2010associated class II molecules. Interestingly, functional class II\u2013peptide complexes were formed at acidic pH 5\u00b75, which restored immune recognition. Acidic buffer (pH 5\u00b75) eluate from <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> cells contained molecules that impaired class II\u2010mediated antigen presentation and CD4<jats:sup>+<\/jats:sup> T\u2010cell recognition. Biochemical analysis showed that these molecules were greater than 30\u00a0000 molecular weight in size, and proteinaceous in nature. In addition, <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> was found to have decreased expression of a 47\u00a0000 molecular weight enolase\u2010like molecule that enhances class II\u2010mediated antigen presentation in B cells, macrophages and dendritic cells, but not in <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> cells. These findings demonstrate that <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> likely has multiple defects in HLA class II\u2010mediated antigen presentation and immune recognition, which may be exploited for future immunotherapies.<\/jats:p>","DOI":"10.1111\/imm.12281","type":"journal-article","created":{"date-parts":[[2014,3,15]],"date-time":"2014-03-15T08:36:38Z","timestamp":1394872598000},"page":"492-505","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Disruption of <scp>HLA<\/scp> class II antigen presentation in Burkitt lymphoma: implication of a 47\u00a0000 MW acid labile protein in CD4<sup>+<\/sup> T\u2010cell recognition"],"prefix":"10.1111","volume":"142","author":[{"given":"Jason M.","family":"God","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology Hollings Cancer Center, and Children's Research Institute Medical University of South Carolina 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