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* University of California San Francisco, San Francisco, CA 94143;
School of Computing, Queen’s University. Kingston, Ontario, Canada;
Monash University, Melbourne, Australia; and
Unidad Experimental Grupo Neurogenética, Hospital Donostia, San Sebastián, Spain
We analyzed global transcriptional changes in the lymph nodes of mice with experimental autoimmune encephalomyelitis in a longitudinal fashion. Most of the transcriptional activity was observed between 3 and 5 days postimmunization. After that period, gene expression changes decayed sharply back to baseline levels. A comparison of transcriptional profiles between immunized and control mice at the time of peak disease activity revealed 266 transcripts, mostly involved in cell-cell interaction and protein synthesis. When the same comparison was performed at the time of recovery from an attack, increased expression of genes coding for milk components were identified. Specifically, casein 
(Csn1s1), 
(Csn2), 
(Csn1s2a), and 
(Csn3), in addition to lactoalbumin and extracellular proteinase were elevated >3-fold in immunized animals compared with CFA-injected controls. We confirmed these findings by quantitative RT-PCR and immunostaining of Csn3. Interestingly, the expression of Csn3 was also found elevated in the blood of multiple sclerosis (MS) patients after a relapse. Altogether, our data suggest that increased production of milk-related transcripts in the lymph nodes and blood succeeds an inflammatory event in experimental autoimmune encephalomyelitis and MS. The potential role of lactogenic hormones in MS is discussed.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This research was supported by The Wasdworth Foundation (to S.E.B.); National MS Society Grants RG2901C6 and CA1035A7 (to J.R.O. and S.E.B.); and grants from MS Research Australia, The Baker Foundation and Towards a Cure, Australia (to C.C.A.B.), Fundación ILUNDAIN, and by the Basque Government (to D.O.).
2 Address correspondence and reprint requests to Dr. Sergio E. Baranzini, 513 Parnassus Avenue, Room S-256, San Francisco, CA 94143-0435. E-mail address: sebaran{at}cgl.ucsf.edu
3 Abbreviations used in this paper: MS, multiple sclerosis; EAE, experimental autoimmune encephalomyelitis; MOG, myelin oligodendrocyte glycoprotein; dpi, days postimmunization; BL, baseline; EE, early EAE; PE, peak EAE; ER, early recovery; LR, late recovery; LN, lymph node; EDSS, Expanded Disability Status Scale; qRT-PCR, quantitative PCR; BTN, butyrophilin; SPMS, secondary progressive multiple sclerosis; OPN, osteopontin; Ltf, lactotransferrin; DEG, differentially expressed gene; CC, class comparison; Lalba, lactoalbumin; Expi, extracellular proteinase inhibitor.
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