Cytokine gene expression following neural grafts

Vine, Alison M.; Lang, Jill; Wood, Matthew; Charlton, H. M.

doi:10.1007/s002210050737

Cited by 9 publications

(5 citation statements)

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“…Young and old LongEvans rats contained similar concentration of TGF-ß 1 mRNA in parietofrontal cortex, midbrain, hypothalamus, hippocampus, and cerebellum [31]. Interestingly, sham operation of mouse caudate nucleus produced minimal upregulation of this and other cytokine mRNA [34]. In contrast, two groups did not detect TGF-ß 1 mRNA in normal rat brain [35,36].…”

Section: Tgf-ß 1 Genementioning

confidence: 73%

“…IL-10 mRNA was detected by RT-PCR 7 days after neural tissue grafting in mouse caudate nucleus. However, since in these studies leukocytes infiltrated the graft area, the precise source of this mRNA is ambiguous [34]. Others did not detect IL-10 mRNA in human [18,53,54], rat [55,56] and mouse [57] brain.…”

Section: Il-10mentioning

confidence: 99%

“…Presence of TGF-ß 1 mRNA was detected by various techniques in CNS in normal human [17][18][19][20], rat [21][22][23][24][25][26][27][28][29][30][31][32] and mouse [33,34] brain. For example, we detected TGF-ß 1 mRNA in rat brain by Northern blotting [21] and in human brain ( fig.…”

Section: Tgf-ß 1 Genementioning

confidence: 99%

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Anti-Inflammatory Cytokines: Expression and Action in the Brain

Vitkoviç

Miyagawa

Sternberg

2001

Neuroimmunomodulation

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Transforming growth factor-β₁ (TGF-β₁) and interleukin (IL)-10 gene expression is equivocal in normal brain and upregulated in over a dozen central and peripheral diseases/disorders. The patterns of specific expression of cytokines differ in these diseases. Published data indicate that these cytokines are produced by and act on both neurons and glial cells. Although their actions are commonly viewed as ‘anti-inflammatory’, they protect neurons and downregulate the responses of glial cells to diseases/disorders in the absence of inflammation. Their actions counterbalance the actions of elevated IL-1 and/or tumor necrosis factor-α to maintain homeostasis. Their therapeutic potential will be realized by improving our understanding of their place in neural cytokine networks.

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Section: Tgf-ß 1 Genementioning

confidence: 73%

Section: Il-10mentioning

confidence: 99%

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Anti-Inflammatory Cytokines: Expression and Action in the Brain

Vitkoviç

Miyagawa

Sternberg

2001

Neuroimmunomodulation

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“…This suggests that common mechanisms operate in this host during rejection of cardiac or neuronal xenografts. It is worth noting that transcripts of Th1 cytokines (IFN‐γ or IL‐2) were reported to accumulate in brains rejecting concordant neurons, in mouse‐to‐rat or rat‐to‐mouse systems (Kogure et al, 1998; Vine et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Temporal analysis of cytokine gene expression during infiltration of porcine neuronal grafts implanted into the rat brain

Melchior

Remy

Nerrière-Daguin

et al. 2002

J of Neuroscience Research

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A large array of evidence supports the involvement of infiltrating T lymphocytes in the rejection process of intracerebral neuronal xenografts. Little is known, however, about the molecular mechanisms that drive the recruitment of this cell type. In the present work, we used real-time RT-PCR methodology to investigate the kinetics of cytokine gene expression during the infiltration of fetal porcine neurons (PNEU) implanted into the striatum of LEW.1A rats. T lymphocyte infiltration was followed by measuring the intracerebral levels of transcripts encoding the beta chain of the T cell receptor. These transcripts remained barely detectable until the fourth week (28 days) postimplantation, when a sudden accumulation occurred. Their kinetics, which support previous immunohistochemical observations, indicate that alphabetaT lymphocyte recruitment occurs rapidly after a delay of several weeks in this experimental model. Infiltration of PNEU grafts by T lymphocytes was accompanied by a concomitant, dramatic augmentation of transcripts coding for monocyte chemotactic protein-1 and RANTES (for regulated on activation, normal T cell expressed and secreted), two chemokines targeting this cell type, among others. Likewise, a sudden accumulation of transcripts of proinflammatory lymphokines [interleukin (IL)-1alpha, tumor necrosis factor-alpha, IL-6] as well as Th1 cytokines (IL-2, interferon-gamma) was also detected. In contrast, IL-4, -10, and -13 mRNA remained barely detectable at the different time points. No significant changes were noticed for IL-12 or transforming growth factor-beta transcripts. These data support the concept that T lymphocyte infiltration of PNEU grafts is actively promoted by a local production of chemokines and proinflammatory lymphokines and is based on a Th1 polarization.

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“…58 All reactions were incubated in a thermal cycler (Techne Genius or Progene) for 30 cycles. The amplification program consisted of an initial denaturation at 951C for 5 min, followed by commencement of the iterative loop: denaturation at 941C for 1 min, annealing at 601C for 1 min, and extension at 721C for 1 min.…”

Section: Rt-pcr and Cdna Synthesismentioning

confidence: 99%

Local adenoviral expression of Fas ligand upregulates pro-inflammatory immune responses in the CNS

et al. 2004

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The central nervous system (CNS) is a site of relative immunological privilege; despite this it can be a target of the immune system under certain conditions. For example, adenoviral vectors elicit an immune response strong enough to result in antigen elimination, in immunologically primed animals. Fas ligand (FasL) contributes to the immune privilege of certain tissues by inducing apoptosis in activated T cells. We therefore investigated whether local overexpression of FasL could downregulate the immune response to adenovirus in the brain. Adenoviral vectors expressing FasL (AdFasL) and the reporter gene b-galactosidase (Adbgal) were co-injected into the striatum of naïve or immunologically primed mice. A co-injection of an adenovirus lacking a transgene (Ad0) and Adbgal acted as a control. At 2 weeks after inoculation, reporter protein expression was significantly reduced with the AdFasL:Adbgal combination compared with the Ad0:Adbgal controls. This was accompanied by a strong inflammatory cell infiltrate, local demyelination and upregulation of pro-inflammatory cytokine gene expression. These experiments demonstrate that FasL overexpression elicits a pro-inflammatory response in the CNS rather than immunosuppression. This was characterized by chronic inflammation and accelerated loss of transgene expression. Induction of such an unexpected pro-inflammatory response caused by introducing FasL may be a peculiarity of the relative immunoprivilege of the unique environment of the brain.

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Cytokine gene expression following neural grafts

Cited by 9 publications

References 0 publications

Anti-Inflammatory Cytokines: Expression and Action in the Brain

Anti-Inflammatory Cytokines: Expression and Action in the Brain

Temporal analysis of cytokine gene expression during infiltration of porcine neuronal grafts implanted into the rat brain

Local adenoviral expression of Fas ligand upregulates pro-inflammatory immune responses in the CNS

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