Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; IgA vs. IgG

JCWinnie,

When can we meet???? You just crack me up! What a sense of humor!

Sharon

Ah-hah! Now I've got her attention.

We could look into each others eyes across the table and I could ask,"Yes, and what about Marker-Hermann and Schwab's article, "
T-cell studies in the spondyloarthropathies," wherein they state:

A growing body of evidence suggests that T lymphocytes play an important role in initiating and maintaining the inflammatory process characteristic of the human leukocyte antigen (HLA)-B27-associated spondyloarthropathies. T cells seem to be involved in the primary defense reaction against arthritis-triggering gram-negative bacteria at the site of extra-articular infection, in determining the systemic cytokine pattern, in the recirculation process between gut mucosa and the joint, and in mediating secondary autoimmune joint inflammation. The factors involved in disease chronicity (namely in ankylosing spondylitis and psoriatic arthritis) are still unknown."""

Curr Rheumatol Rep. 2000 Aug;2(4):297-305.

Best regards,

jcwinnie


Cue "Stangers in the Night"

1: J Leukoc Biol 2001 Nov;70(5):821-9

Effect of cross-tolerance between endotoxin and TNF-alpha or IL-1beta on cellular signaling and mediator production.

Ferlito M, Romanenko OG, Ashton S, Squadrito F, Halushka PV, Cook JA.

Department of Physiology and Neuroscience, Medical University of South Carolina, Charleston, USA.

Endotoxin [lipopolysaccharide (LPS)] tolerance suppresses macrophage/monocyte proinflammatory-mediator production. This phenomenon also confers cross-tolerance to other stimuli including tumor necrosis factor (TNF) alpha and interleukin (IL)-1beta. Post-receptor convergence of signal transduction pathways might occur after LPS, IL-1beta, and TNF-alpha stimulation. Therefore, it was hypothesized that down-regulation of common signaling molecules induces cross-tolerance among these stimuli. LPS tolerance and cross-tolerance were examined in THP-1 cells. Phosphorylation of MAP kinases and degradation of inhibitor kappaBalpha (IkappaBalpha) DNA binding of nuclear factor-kappaB (NF-kappaB), and mediator production were examined. In naive cells, LPS, TNF-alpha, and IL-1beta induced IkappaBalpha degradation, kinase phosphorylation, and NF-kappaB DNA binding. LPS stimulation induced production of TNF-alpha or TxB2 and degradation of IRAK. However, neither TNF-alpha nor
IL-1beta induced IRAK degradation or stimulated TNF-alpha or TxB2 production in naive cells. Pretreatment with each stimulus induced homologous tolerance to restimulation with the same agonist. LPS tolerance also suppressed LPS-induced TxB2 and TNF-alpha production. LPS pretreatment induced cross-tolerance to TNF-alpha or IL-1beta stimulation. Pretreatment with TNF-alpha induced
cross-tolerance to LPS-induced signaling events and TxB2 production. Although pretreatment with IL-1beta did not induce cross-tolerance to LPS-induced signaling events, it strongly inhibited LPS TNF-alpha and TxB2 production. These data demonstrate that IL-1beta induces cross-tolerance to LPS-induced mediator production without suppressing LPS-induced signaling to MAP kinases or NF-kappaB activation.

PMID: 11698503 [PubMed - indexed for MEDLINE]

& Evelyn says, "Huh?"

Best regards,

jcwinnie

(no picture could describe it)