Adding a bit to what mrsD has explained:

Antibodies are made by blood cells called plasma cells which are produced from B lymphocytes (B cells). Each clone of B cells and plasma cells produces a unique kind of antibody.

Production of plasma cells needs help from a class of T lymphocytes called helper T cells. Helper T cells need to get activated before they can do their job. This happens when they recognise a complex of a peptide (a small part of a protein) bound to Class II MHC proteins on cells called antigen-presenting cells. There are many different kinds of Class II MHC proteins - everybody inherits a specific pattern of them from their parents.

Usually that peptide is derived from a protein made by a pathogen (virus, bacterium, etc). Most often clones of helper T cells get specifically activated by recognising a peptide:Class II MHC complex. They go on to activate specific clones of B cells with the same peptide:Class II MHC complex on their cell surfaces. The plasma cells derived from them secrete specific antibodies which lead to destruction of the pathogen which made the protein.

However, sometimes this goes wrong. A combination of pathogen peptide:Class II MHC protein might, in a chemical sense, "look like" a combination of normal body cell peptide:Class II MHC protein. The effect of this is that the immune system will damage the normal body cells which made that peptide, "thinking" that those cells are pathogens - this is an auto-immune disease.

Inheritance of a specific pattern of Class II MHC proteins is often a risk factor for specific auto-immune diseases. For example, inheritance of forms of a Class II MHC protein called HLA-DRB1 is a risk factor for RA. Presumably this is because complexes of pathogen peptide:HLA-DRB1 can "look like" complexes of joint tissue peptides and HLA-DRB1, leading to immune system damage of joint tissue.

I hope that this is not too complicated and makes sense.