Biomedical Engineering Reference
In-Depth Information
• CD4 T cells are helper T lymphocytes; they recognize peptide antigens
resented by MHC II molecules on professional antigen-presenting cells
(macrophages, dendritic cells, B cells).
• CD8T cells are cytotoxic T lymphocytes; they recognize peptide antigens
presented by MHC I molecules.
• CD1-MHC I-b
type of glycoproteins are non-classical type I MHC-
like molecules (found on monocytes/macrophages, some B cells, and
thymocytes), which present lipid antigens to NKT cells.
CAMs AND I/R INJURY
Based on the paucity of information about changes in CAMs during DCS other
than our own study (Bigley
et al.
2008), we examined the features of another well-
known model (I/R injury) of tissue hypoxia leading to changes in CAMs. In a
murine hindlimb ischemia model, endothelial progenitor cells homed to and
bound to endothelial cells through ICAM-1/β-2 integrin interaction; ICAM-1
was overexpressed on ischemic muscle (Yoon
et al.
2006). As shown in Table 2,
lymphocyte function-associated antigen (LFA-1), a ligand for ICAM-1, and very
late antigen 4 (VLA-4), a ligand for VCAM-1, are involved in vasoendothelial
adhesion and transendothelial migration of high proliferative potential
endothelial progenitor cells to ICAM-1/2 and VCAM-1 expressing bone marrow
endothelial cells (Duan
et al.
2006, 2008). Endothelial cell expression of ICAM-
1/2 and VCAM-1 increased at er activation with cytokines IL-1β and TNF-α (8).
Duan
et al.
observed that LFA-1 and VLA-4 are involved in the homing of these
progenitor cells to ischemic tissues. Anti-ICAM-1 antibody ef ectively inhibited
early inl ammatory processes and reperfusion-induced injury in a rat middle
cerebral artery occlusion model and in lung (Kanemoto
et al.
2002, Chiang
et al.
2006). Anti-TNF-α antibody has therapeutic and preventive ef ects on I/R lung
injury (Chiang
et al.
2006).
h e signii cance of these CAMs and the complexity of the cells and molecules
(Table 4)
involved in inl ammation in acute kidney injury are highlighted by
Kinsey and Okusa (2008). Ischemia-reperfusion is the traumatic event inducing
changes in endothelia, leukocytes and renal tubular epithelial cells and involves
a variety of bone marrow-derived cells, endothelia, epithelia, and complement
pathways contributing to hypoxia
(Tables 4 and 5).
Ischemia-reperfusion injury
is a major problem in intestinal (Watson
et al.
2008), heart (Haverslag
et al.
2008,
Lange
et al.
2008) and lung transplantation (Ellman
et al.
2008, Zang
et al.
2009).
It is an important factor in morbidity and mortality following lung transplantation
(Zang
et al.
2009). In renal transplantation, increased expression of ICAM-1
appears to be an early marker of acute rejection (Kinsey and Osuka 2008). In
a mouse model of cardiac isograt s, ICAM-1 mRNA peaked at 3 hr following
