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Laboratory of Molecular Immunology, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115
Both clinical and experimental observations suggest that allograft
rejection is a complex process with multiple components that are, at
least partially, functionally redundant. Studies using graft recipients
deficient in various genes including chemokines, cytokines, and other
immune-associated genes frequently produce a phenotype of delayed, but
not indefinitely prevented, rejection. Only a small subset of genetic
deletions (for example, TCR
or 
, MHC I and II, B7-1 and B7-2, and
recombinase-activating gene) permit permanent graft acceptance
suggesting that rejection is orchestrated by a complex network of
interrelated inflammatory and immune responses. To investigate this
complex process, we have used oligonucleotide microarrays to generate
quantitative mRNA expression profiles following transplantation.
Patterns of gene expression were confirmed with real-time PCR data.
Hierarchical clustering algorithms clearly differentiated the early and
late phases of rejection. Self-organizing maps identified clusters of
coordinately regulated genes. Genes up-regulated during the early phase
included genes with prior biological functions associated with
ischemia, injury, and Ag-independent innate immunity, whereas genes
up-regulated in the late phase were enriched for genes associated with
adaptive immunity.
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