If you try hard enough you can find a weak link between lectins and AS through a few degrees of separation via H.Pylori.

H. pylori has a special affinity for glycoproteins. It acts by binding to several essential sugars, in particular mannose, fucose and glucosamine. The mucous lining in the stomach is designed to prevent such infections by providing essential sugars onto which the bacteria can attach and be washed away, rather than allowing it to attach to the sugars in the stomach wall. Dietary lectins, particularly ones that react with mannose as well as fucose and glucosamine (wheat, corn, potatoes, lentils etc) work by stripping away this essential mucous in vulnerable individuals and allowing h. pylori to gain a foothold into the stomach lining. - http://www.plantpoisonsandrottenstuff.info/content/toxins/essential-sugars-plant-lectins.aspx

In this study H.Pylori was found in 73% of SpA patients and only 27% of the controls - http://content.karger.com/ProdukteDB/pro...roduktNr=224269

So increased lectin consumption increases the risk of H.Pylori and H.Pylori has been found to be almost three times more prevelant in SpA patients than the regular population.

Also ... "Eating too many lectin-containing foods or catching a lectin-producing pathogen can lead to autoimmune disease. It is frequently observed that autoimmune conditions (where the body mistakenly attacks itself) often arise after a serious infection. Rheumatoid arthritis, multiple sclerosis, Guillian-Barre syndrome, Type 1 diabetes, and a whole host of other autoimmune conditions are associated with both infections and with eating lectin-containing foods. It is thought that lectins work by stripping away certain essential sugars from cell surfaces, making them display incorrect antigens and appear to be foreign to the body's immune system. They may also work simply by binding irreversibly to particular cells or proteins, forcing them to be taken out of circulation by white blood cells. These are the mechanisms through which coeliac (celiac) disease is thought to be mediated. Food allergies may also be mediated by lectins.

Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells. The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetylgalactosamine, which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together---a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice. Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.

The good news is that the effects of dietary lectins only extend for as long as they are in the body, and the effects of both dietary and pathogen produced lectins can be reduced with supplementation of essential sugars. Furthermore some lectins in foods can be reduced (but not eliminated) by a variety of methods." - http://www.plantpoisonsandrottenstuff.info/content/toxins/essential-sugars-plant-lectins.aspx

I'm still on the fence about these lectins but it is certainly worthy of further investigation. It is also curious that a low starch diet is also a low lectin diet as almost all of the lectin containing foods are starchy.