Hoedemaekers A - Search Results

1

Differential susceptibility of young and old rat neuromuscular junctions to antibody-mediated AChR degradation in experimental autoimmune myasthenia gravis.

Hoedemaekers A, Bessereau JL, Graus Y, Guyon T, Changeux JP, Berrih-Aknin S, Van Breda Vriesman P, De Baets M. Hoedemaekers A, et al. Ann N Y Acad Sci. 1998 May 13;841:550-4. doi: 10.1111/j.1749-6632.1998.tb10981.x. Ann N Y Acad Sci. 1998. PMID: 9668293 No abstract available.

2

Hoedemaekers A, Graus Y, van Breda Vriesman P, de Baets M. Hoedemaekers A, et al. Clin Exp Immunol. 1997 Jan;107(1):189-97. doi: 10.1046/j.1365-2249.1997.d01-881.x. Clin Exp Immunol. 1997. PMID: 9010275 Free PMC article.

3

Macrophage infiltration at the neuromuscular junction does not contribute to AChR loss and age-related resistance to EAMG.

Hoedemaekers A, Graus Y, Beijleveld L, van Breda Vriesman P, De Baets M. Hoedemaekers A, et al. J Neuroimmunol. 1997 May;75(1-2):147-55. doi: 10.1016/s0165-5728(97)00016-7. J Neuroimmunol. 1997. PMID: 9143248

4

Role of the target organ in determining susceptibility to experimental autoimmune myasthenia gravis.

Hoedemaekers A, Bessereau JL, Graus Y, Guyon T, Changeux JP, Berrih-Aknin S, van Breda Vriesman P, De Baets MH. Hoedemaekers A, et al. J Neuroimmunol. 1998 Aug 14;89(1-2):131-41. doi: 10.1016/s0165-5728(98)00126-x. J Neuroimmunol. 1998. PMID: 9726835

5

Hoedemaekers AC, Verschuuren JJ, Spaans F, Graus YF, Riemersma S, van Breda Vriesman PJ, De Baets MH. Hoedemaekers AC, et al. Muscle Nerve. 1997 Sep;20(9):1091-101. doi: 10.1002/(sici)1097-4598(199709)20:9<1091::aid-mus1>3.0.co;2-3. Muscle Nerve. 1997. PMID: 9270663

6

Myasthenia gravis as a prototype autoimmune receptor disease.

Hoedemaekers AC, van Breda Vriesman PJ, De Baets MH. Hoedemaekers AC, et al. Immunol Res. 1997;16(4):341-54. doi: 10.1007/BF02786398. Immunol Res. 1997. PMID: 9439759 Review.

7

Coimmunization of MHC class II competitor peptides during experimental autoimmune myasthenia gravis induction resulted not only in a suppressed, but also in an altered immune response.

Wauben MH, Hoedemaekers AC, Graus YM, Wagenaar JP, Van Eden W, De Baets MH. Wauben MH, et al. Among authors: hoedemaekers ac. Ann N Y Acad Sci. 1998 May 13;841:338-41. doi: 10.1111/j.1749-6632.1998.tb10942.x. Ann N Y Acad Sci. 1998. PMID: 9668254 No abstract available.

8

Inhibition of experimental autoimmune myasthenia gravis by major histocompatibility complex class II competitor peptides results not only in a suppressed but also in an altered immune response.

Wauben MH, Hoedemaekers AC, Graus YM, Wagenaar JP, van Eden W, de Baets MH. Wauben MH, et al. Among authors: hoedemaekers ac. Eur J Immunol. 1996 Dec;26(12):2866-75. doi: 10.1002/eji.1830261210. Eur J Immunol. 1996. PMID: 8977279

9

Polarization toward the T-helper(Th)1 type immune response is not required for rat experimental autoimmune myasthenia gravis.

Saoudi A, Bernard I, Hoedemaekers A, Cautain B, Martinez K, Druet P, De Baets M, Guéry JC. Saoudi A, et al. Among authors: hoedemaekers a. Transplant Proc. 1999 May;31(3):1604-5. doi: 10.1016/s0041-1345(99)00055-x. Transplant Proc. 1999. PMID: 10331019 No abstract available.

10

Experimental autoimmune myasthenia gravis may occur in the context of a polarized Th1- or Th2-type immune response in rats.

Saoudi A, Bernard I, Hoedemaekers A, Cautain B, Martinez K, Druet P, De Baets M, Guéry JC. Saoudi A, et al. Among authors: hoedemaekers a. J Immunol. 1999 Jun 15;162(12):7189-97. J Immunol. 1999. PMID: 10358165

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