Soluble form of an HLA-B7 class I antigen specifically suppresses humoral alloimmunization

Analysis of endogenous peptides bound by soluble MHC class I molecules: a novel approach for identifying tumor-specific antigens

“…Purification of peptides from sHLA was previously achieved by truncating its entire transmembrane and cytoplasmic domains 21, by using a non‐functional transmembrane domain such as Q10 b 22 or by fusing the extra‐cellular domains to soluble secreted proteins such as Fc domains of antibodies 23. Such sHLA were produced in cultured cells 21, 24, 25 and were demonstrated to bind their cognate TCR, indicating that they maintain their native structure including the presence of endogenous peptides that mediate this interaction 26, 27. Analysis of bound peptides recovered from the secreted murine MHC H‐2L d was performed by Edman sequencing 28 and more recently by ESI‐MS/MS 25, 29.…”

Behavior of serum human major histocompatibility complex class I antigen levels in human immunodeficiency virus-infected patients during antiretroviral therapy: Correlation with clinical outcome

“…The inhibitory effects of sHLA-I antigens on CTLs may occur through multiple mechanisms, including receptor blockade, binding to CD8 molecules via their ␣ 3 domain, and induction of apoptosis [25][26][27]. Furthermore, the report that a genetically engineered sHLA-B7 molecule can induce specific tolerance suggests an additional mechanism by which circulating HLA-I antigens can modulate immune responses [32]. Therefore, the decrease of sHLA-I serum level detectable in the course of HAART treatment could positively affect CTL response, favoring their cytotoxic activity against pathogens.…”

The soluble form of human leukocyte antigen class I antigen causes apoptosis on hepatocellular carcinoma cell lines

“…Thus, the alternative splicing form excreted outside the cells plays some role in controlling the extent of the immune reaction. Whereas many reports have discussed the relationship between sHLA-I and the immune reaction (5)(6)(7)(8)(9)(10), only a few have discussed its biological significance in malignancy (19,29). We have reported that the level of sHLA-I in far-advanced gastric cancer patients was significantly lower than that in a normal control and in the early stages of cancer (19).…”

“…Reports indicate that it increases in an immunologically activated status, e.g. in autoimmune diseases, such as systemic lupus erythematosus (5) and rheumatoid arthritis (6), as well as after transplantation (7)(8)(9)(10). The liver is considered to be a major organ for producing sHLA-I (11).…”