Type II collagen (CII) is a candidate cartilage‐specific autoantigen, which can become post‐translationally modified by hydroxylation and glycosylation. T cell recognition of CII is essential for the development of murine collagen‐induced arthritis (CIA) and also occurs in rheumatoid arthritis (RA). The common denominator of murine CIA and human RA is the presentation of an immunodominant CII‐derived glycosylated peptide on murine A^q and human DR4 molecules, respectively. To investigate the importance of T cell recognition of glycosylated CII in CIA development after immunization with heterologous CII, we treated neonatal mice with different heterologous CII‐peptides (non‐modified, hydroxylated and galactosylated). Treatment with the galactosylated peptide (galactoseat position 264) was superior in protecting mice from CIA. Protection was accompanied by a reduced antibody response to CII and by an impaired T cell response to the glycopeptide. To investigate the importance of glycopeptide recognition in an autologous CIA model, we treated MMC‐transgenic mice, which express the heterologous CII epitope with a glutamic acid in position 266 in cartilage, with CII‐peptides. Again, a strong vaccination potential of the glycopeptide was seen. Hence CII‐glycopeptides may be the optimal choice of vaccination target in RA, since humans share the same epitope as the MMC mouse.