Chronic Immune Complex Disease: Behavioral and Immunological Correlates

Abstract

Using a fear avoidance paradigm, behavioral effects were seen in Sprague-Dawley rats in which chronic immune complex disease was induced. These effects were related to changes in urine protein that developed during the course of the experiment. Experimental animals also had glomerular deposits of rat gamma globulin and BSA as determined by immunofluorescence; C3 deposits were observed in half of these animals. BSA and/or rat gamma-globulin, but not C3, was seen in the choroid plexus of half of the experimental animals. This is the first study to report behavioral changes associated with the induction of chronic immune complex disease in experimental animals.

Autoantibodies, immune complexes, and behavioral disorders: Neuropsychiatric involvement in systemic lupus erythematosus

“…Since it is known that there are immune complex deposits in the choroid plexus of patients with SLE, as well as in animal models Hoffman et al, 1978a;Koss et al, 1973;Lampert and Oldstone, 1973;Morgan et al, 1977;Peress et al, 1977a;Peress and Tompkins, 19791, it is important to determine whether immune complexes can alter BBB permeability and in this way lead to some of the neuropsychiatric manifestations seen in this disease. It is feasible that BBB permeability changes, induced by immune complexes, could lead to altered behavior by changing cerebrospinal fluid, or extracellular fluid composition, by allowing autoantibodies or immune complexes to get into the CNS, or by making it easier for cells of the immune system to enter the CNS.…”

DLK: The “Preconditioning” Signal for Axon Regeneration?

“…The loss of DLK abolished any response to a preconditioning injury (Figure 1). The only preconditioning effect not mimicked by DLK seems to be the shortened latency to growth cone formation, but Shin et al (2012) did not directly address whether there was a change in latency after a preconditioning injury in their experiments (Hoffman, 2010).…”

“…Is DLK the signaling molecule responsible for the improved axon regeneration induced by a preconditioning injury? Wild-type sensory axons respond to a preconditioning injury with an accelerated regeneration after a second injury (McQuarrie and Grafstein, 1973;Hoffman, 2010). Shin et al (2012) found that this conditioning injury effect was completely abolished in DLK KO sciatic sensory axons in vivo.…”

“…Peripheral nervous system (PNS) axons luckily do regenerate and mount a robust response because of an intrinsic regeneration program. This cell-intrinsic regeneration program (thought to be a reactivation of the developmental program) is turned on by a retrograde injury signal that activates a transcriptional program ( Figure 1) (Cavalli et al, 2005;Hoffman, 2010;Liu et al, 2011). The difference between CNS and PNS neuron regeneration abilities is thought to be due to two factors: an ''inhibitory'' CNS environment and a ''weak'' activation of the intrinsic regeneration program.…”

“…Much research has gone into identifying the molecular mechanisms responsible for the improved regeneration associated with a preconditioning injury (Hoffman, 2010). The cell-intrinsic regen-eration program is dependent on transcription factors activated by a retrograde injury signal delivered to the cell body (Cavalli et al, 2005;Liu et al, 2011).…”