Disease relevance of Cd69

• This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line [1].
• Milk transmission of virus led to higher virus titers and lymphoma incidence in B10.A (H-2a) mice than in B10 (H-2b) mice, and the latter strain produced higher titers of anti-VEA antibodies than did the former [2].
• A subset of CD4+ T cells expressing early activation antigen CD69 in murine lupus: possible abnormal regulatory role for cytokine imbalance [3].
• The CD69 antigen is the earliest activation marker expressed on leukocyte surfaces after stimulation and it has been correlated with disease state in a variety of inflammatory and autoimmune diseases [4].

High impact information on Cd69

• The failure of B10.A V+ mice to produce IgG antibodies against VEA was not due to an intrinsic defect of helper T-cell function because these mice produced IgG antivirus antibodies after sc immunization with killed viral vaccine [2].
• In C57BL mice milk-borne infection with B-tropic murine leukemia virus (V+ denoting positive for milk-transmitted B-tropic virus and V- denoting negative for milk-transmitted B-tropic virus) was accompanied by an antibody response against viral envelope antigens (VEA) [2].
• Nevertheless, CD69-deficient lymphocytes had a normal proliferative response to different T-cell and B-cell stimuli [5].
• Together, these observations indicate that CD69 plays a role in B-cell development and suggest that the putative stimulatory activity of this molecule on bone marrow-derived cells may be replaced in vivo by other signal transducing receptors [5].
• AIM/CD69 is the earliest leukocyte activation antigen and is expressed mainly by activated T, B, and natural killer (NK) cells [5].

Biological context of Cd69

• Phenotypic and functional characteristics of hematopoietic cell lineages in CD69-deficient mice [5].
• The engagement of CD69 by specific antibodies induces intracellular signals, including Ca(++) flux, cytokine synthesis, and cell proliferation [5].
• Segregation analysis of an informative family of hybrids followed by molecular and karyotype studies clearly demonstrated that the locus encoding CD69 antigen mapped to human chromosome 12 [6].
• A single pulse with hybrid antibodies rescues immature, CD4/8 double-positive thymocytes from their programmed death in vivo, induces expression of the early activation antigen CD69 followed by TcR up-regulation, concomitant down-regulation of CD8 or CD4 and their conversion to functional mature T cells by day 3 [7].
• When oocytes were injected with spermatozoa preserved in ETBS supplemented with DMSO or VEA/DMSO, chromosome integrity did not decrease significantly (through 9 days of preservation) [8].

Anatomical context of Cd69

• Furthermore, studies of negative- and positive-thymocyte selection using a T-cell receptor transgenic model demonstrated that these processes were not altered in CD69 (-/-) mice [5].
• In addition, natural killer and cytotoxic T lymphocyte cells from CD69-deficient mice displayed cytotoxic activity similar to that of wild-type mice [5].
• CD69 (-/-) mice showed largely normal hematopoietic cell development and normal T-cell subpopulations in thymus and periphery [5].
• To investigate the physiological relevance of CD69, we generated mice deficient in CD69 (CD69-/-) by gene targeting in embryonic stem cells [5].
• Expression and function of the early activation antigen CD69 in murine macrophages [9].

Other interactions of Cd69

• The B220(hi)IgM(neg) bone marrow pre-B cell compartment was augmented in CD69 (-/-) mice [5].
• During primary and secondary responses, expression of 4-1BB on in vivo-activated TCR transgenic T cells was earlier and more transient than previously observed in vitro, correlating with expression of the early activation antigen CD69 and preceding the transition to the CD44hi state [10].

Analytical, diagnostic and therapeutic context of Cd69

• Genomic sequence analysis indicates the presence of at least seven members between Nkrpla and Cd69 [11].
• After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts [1].

References