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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Interleukin-1-related activity and hypocretin-1 in cerebrospinal fluid contribute to fatigue in primary Sjögren’s syndrome

Fig. 2

Hypothetical model for fatigue. Danger signals activate astroglia to produce and release S100B that bind to TLR4 and RAGE receptors on microglia. Activated microglia produce IL-1β that bind specific receptors (IL-1R1/IL-1RAcPb) on neurons and induce sickness behavior. There are no specific receptors for IL-6 that can modulate neurons in the same manner as for IL-1β, but higher levels of IL-6 may through stimulation of TNFα synthesis reduce the amount of Hcrt-1 in neurons. Low levels of Hcrt-1 can lead to or modulate fatigue through unknown pathways

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