Several statistically significant probes with higher hybridization signals in Jurkat cells, such as those for [CD2.sup.5] CD3E, LCK, GZMA, and CD28, represented genes related to T lymphocytes (24-26).
 Human genes: CD2, CD2 molecule; CD3E, CD3e molecule, e (CD3-TCR complex); LCK, lymphocyte-specific protein tyrosine kinase; GZMA, granzyme A (granzyme 1, cytotoxic T-lymphocyte-associated serine esterase 3); CD28, CD28 molecule; MNDA, myeloid cell nuclear differentiation antigen; LYN, v-yes-1 Yamaguchi sarcoma viral related oncogene homolog; MYC, v-myc myelocytomatosis viral oncogene homolog (avian); BTG1, B-cell translocation gene 1, anti-proliferafive; CD79A, CD79a molecule, immunoglobulin-associated a; FAIM3, Fas apoptotic inhibitory molecule 3; CCR7, chemokine (C-C mofif) receptor 7; CD48, CD48 molecule; HLA-DRA, major histocompatibility complex, class II, DR a; FCER2, Fc fragment of IgE, low affinity II, receptor for (CD23); CD52, CD52 molecule.
The most abundant gzms, gzmA and gzmB, are constitutively expressed in several cell types including cytotoxic T lymphocytes (CTL), natural killer (NK) cells, NKT cells, and [gamma][delta] T cells [6, 7]; their expression has been also observed in other cell types, including nonlymphoid cells, at least after stimulation [8, 9].
In the present study, we aimed to investigate the role of gzmA and gzmB in the host response to E.
To analyze the basal levels of gzmA and gzmB, groups of WT mice were euthanized before and after infection with E.