Out of the FOXP transcriptional factor family that includes FOXP1, FOXP2, and FOXP3, only FOXP3 has the ability to inhibit IL-2, IL-4, and IFN- production by primary T-helper cells. IL-2, IL-4, and IFN-gamma are cytokines that promote type 1 and type 2 response. As it was mentioned in your post, in humans, forced expression of FOXP3 significantly suppresses endogenous cytokine expression driven by NFAT and NF-kB – factors involved in the activation of the immune and inflammatory responses in T lymphocytes. As a result, FOXP3 mutations cause X-linked autoimmunity-allergic disregulation syndrome. Mutation in FOXP2 on the other hand, although it belongs to the same factor family, has been linked to speech-language disorder, which suggests its role in neural development. Children with impaired FOXP2 have typical phenotype. First of all, they show signs of CAS (childhood apraxia of speech) – disorder of speech motor programming or planning, which affects the production, sequencing, timing, and stress of sounds, syllables, and words that an individual tries to pronounce. Regardless of the underlying cause of CAS, affected people experince difficulties in automatically and accurately sequencing speech sounds into syllables, syllables into words, and words into sentences with the correct prosody. Another symptoms of mutations in FOXP2 include oral motor dyspraxia (difficulty in planning or programming oral movements on command), dysarthria (a disorder affecting nasal resonance, voice quality, prosody, and breath support for speech), receptive and expressive language disorder that can be moderate or severe, and reading and spelling impairments.