Cytotoxic treatment with rabbit antiserum raised against purified glycosphingolipid "asialo GM1" was capable of eliminating natural killer (NK) activity of spleen cells from different inbred mouse strains including CBA/J, C57BL/6, BALB/c, AKR, and athymic nude mice. The anti-asialo GM1 antiserum showed little cross-reactivity with structurally related glycolipids, e.g. GM), GD 1 b and asialo GM2 in the microflocculation test. The specific reactivity of this antiserum with NK cells was confirmed by the quantitative absorption of anti-NK activity with graded amounts of asialo GM1 but not with other glycosphingolipids. The absorption of anti-brain-associated T cell antigen (anti-BAT) with asialo GM1 also effectively diminished its anti-NK activity, leaving the ability to kill T cells intact. This suggests that the antibody to asialo GM1 is responsible for the anti-NK activity contained in the anti-BAT antiserum. In contrast to the extreme sensitivity of NK cells to anti-asialo GM1, alloreactive cytotoxic T killer cells generated in the mixed lymphocyte culture were not killed by anti-asialo GM1 and complement. These results indicate that asialo GM1 is expressed on mouse NK cells in a high concentration.

Mice require testicular glycosphingolipids (GSLs) for proper spermatogenesis. Mutant mice strains deficient in specific genes encoding biosynthetic enzymes of the GSL pathway including Galgt1 (encoding GM2 synthase) and Siat9 (encoding GM3 synthase) have been established lacking various overlapping subsets of GSLs. Although male Galgt1؊/؊ mice are infertile, male Siat9؊/؊ mice are fertile. Interestingly, GSLs thought to be essential for male spermatogenesis are not synthesized in either of these mice strains. Hence, these GSLs cannot account for the different phenotypes. A novel class of GSLs was observed composed of eight fucosylated molecules present in fertile but not in infertile mutant mice. These GSLs contain polyunsaturated very long chain fatty acid residues in their ceramide moieties. GSLs of this class are expressed differentially in testicular germ cells. More importantly, the neutral subset of this new GSL class strictly correlates with male fertility. These data implicate polyunsaturated, fucosylated GSLs as essential for spermatogenesis and male mouse fertility.

H¢lic~baeter pylorl has I~en identified as a ¢~ttaati~ a=enl in ,ctiw chronic $astritis, The rec=ptor for this baeteri=t, however, is not known, It is likely that the r~wptor molecules may b~ 81yt:osphinsolipid~.* as shown in th~ ea~cs orother bacteria. We explored this po~sihility by a thin-layer chromatography (~LC).immun~staininu method. Amontt lllyeo~phinllolipids extracted from hum;tn gastric mucosa, intact t1¢11¢.oba¢l¢t pylorl Sl~.cifleall~, bound to PSO~.O~tleer trod IPNeuAc.LacCer. whereas no specific bindin8 to neutral tll~sphint~olipids, ,,vhiel~ sh~re the same ¢era mide muiety with P$Os-OalCer or ! PNeuAe. LacCer, was demonstrated, $onieated bacteria could still bind to I PNeoAoLacCer with comparable affinity. In contrast, the btndinll of bacteria to PSO~.GaiCer was 8reatly diminished upon sonieation, Th~se results suS$est that each of the olisosaeehar.ide moieties mr I PNeuAc-LacCcr and PSO,-GalCer may be spccitlcally recol]nized by difl'eren~ liljand molecule= of llelieaba¢ter i)~,'larLH¢lirc~harr¢r pylorl: Gastric mucosa: Glycosphinsolipid; Bacterial adhesion

No abstract

Serum antibody from some patients with Guillain-Barré syndrome recognized an antigen of a minor component in human brain monosialoganglioside fraction. We purified that antigen, which migrated at a position slightly lower than that of GM1 on a thin-layer chromatogram (TLC), by using Iatrobeads column chromatography and preparative TLC. Structural analyses, including fast atom bombardment mass spectrometry, showed it to be GM1b. An enzyme-linked immunosorbent assay (ELISA) using purified GM1b showed that anti-GM1b antibody was present in 22 of 104 cases tested. No anti-GM1b antibody was present in the sera from control patients with other diseases or from the normal controls. Four sera recognized only GM1b among the 11 ganglioside antigens tested. The other 18 sera had antibodies to other antigens, most of which shared no terminal epitope with GM1b. Eight of nine sera samples with anti-GalNAc-GD1a antibody also had anti-GM1b antibody. Antibody to a minor monosialoganglioside, GM1b, was found to be a useful diagnostic marker for Guillain-Barré syndrome. Further study is needed to determine whether this antibody plays a role in the pathogenetic mechanism of the syndrome.