title: Constitutive and mitogen-stimulated cytokine mRNA expression by peripheral blood mononuclear cells from most autologous and allogeneic bone marrow transplant recipients is intact.
abstract: The immunodeficiency that occurs after human bone marrow transplantation (BMT) leaves BMT recipients susceptible to fatal infections. Although cytokines are critical for coordinating immune responses and immune reconstitution after BMT, there are still gaps in our knowledge about the expression of mRNA for cytokines in peripheral blood mononuclear cells (PBMC) after BMT. Therefore, we systematically studied cytokine gene expression by PBMC from 11 allogeneic and four autologous BMT recipients from 111 to 837 days after BMT and compared the results with PBMC from seven normal controls tested in parallel. PBMC were examined for mRNA expression for IL-2r alpha, IL-2, IL-3, IL-4, IL-6, and IL-7 using reverse transcription polymerase chain reaction (RT/PCR). PBMC from 11 allogeneic recipients constitutively expressed mRNA for IL-2r alpha in 2 of 11 and IL-2 in 1 of 9 samples tested whereas the same PBMC constitutively expressed mRNA for IL-3 in 8 of 11, IL-4 in 3 of 7, IL-6 in 6 of 7 and IL-7 in 3 of 6 samples tested. After PHA/PMA stimulation, PBMC from the same recipients frequently expressed mRNA for IL-2r alpha in 9 of 11, IL-2 in 8 of 9, IL-4 in 3 of 7 and IL-6 in 7 of 7. PBMC from four autologous recipients (two short-term and two long-term) frequently constitutively expressed mRNA for IL-2r alpha (3 of 4) IL-2 (3 of 4), and IL-3 (4 of 4). Stimulation of PBMC from the autologous recipients did not alter cytokine expression.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Wayne State University, Detroit.
authors.forename: L G
authors.initials: LG
authors.lastname: Lum
authors.forename: I D
authors.initials: ID
authors.lastname: Joshi
authors.forename: M R
authors.initials: MR
authors.lastname: Smith
authors.forename: V
authors.initials: V
authors.lastname: Ratanatharathorn
authors.forename: S C
authors.initials: SC
authors.lastname: Galoforo
authors.forename: C
authors.initials: C
authors.lastname: Karanes
authors.forename: J P
authors.initials: JP
authors.lastname: Uberti
authors.forename: L L
authors.initials: LL
authors.lastname: Sensenbrenner
mesh_terms: D000741:Anemia, Aplastic / Q000628:therapy; D001483:Base Sequence; D016026:Bone Marrow Transplantation / Q000473:pathology*; D016207:Cytokines / Q000235:genetics*; D006801:Humans; D007376:Interleukin-2 / Q000235:genetics; D007377:Interleukin-3 / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D015851:Interleukin-7 / Q000235:genetics; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000628:therapy; D007963:Leukocytes, Mononuclear / Q000737:chemistry / Q000473:pathology* / Q000502:physiology; D008934:Mitogens / Q000494:pharmacology*; D008969:Molecular Sequence Data; D009190:Myelodysplastic Syndromes / Q000628:therapy; D010641:Phenotype; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis* / Q000235:genetics; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous
chemical_list: D016207:Cytokines; D007376:Interleukin-2; D007377:Interleukin-3; D015850:Interleukin-6; D015851:Interleukin-7; D008934:Mitogens; D012333:RNA, Messenger; D015847:Interleukin-4