Below are a collection of excerpts from biomedical research articles. Excerpts are separated by newlines. Your task is to answer a question based these excerpts. Your response should be formatted as a `json` array.

For instance, given excerpts from articles studying breast cancer, and the question "what are some common genes associated with breast cancer?", an answer might be formatted like: ["BRCA1", "BRCA2", "TP53", ...]. Only include answers that are mentioned in the provided exerpts. The array should always have at least one answer; do not respond with an empty array []. Do not include any text in your response other than the answer array.

Context: The transcriptional programs that guide lymphocyte differentiation depend on the precise expression and timing of transcription factors (TFs). The TF BACH2 is essential for T and B lymphocytes and is associated with an archetypal super-enhancer (SE). Single-nucleotide variants in the BACH2 locus are associated with several autoimmune diseases, but BACH2 mutations that cause Mendelian monogenic primary immunodeficiency have not previously been identified. Here we describe a syndrome of BACH2-related immunodeficiency and autoimmunity (BRIDA) that results from BACH2 haploinsufficiency. Affected subjects had lymphocyte-maturation defects that caused immunoglobulin deficiency and intestinal inflammation. The mutations disrupted protein stability by interfering with homodimerization or by causing aggregation. We observed analogous lymphocyte defects in Bach2-heterozygous mice. More generally, we observed that genes that cause monogenic haploinsufficient diseases were substantially enriched for TFs and SE architecture. These findings reveal a previously unrecognized feature of SE architecture in Mendelian diseases of immunity: heterozygous mutations in SE-regulated genes identified by whole-exome/genome sequencing may have greater significance than previously recognized.

Question:
What is caused by BACH2-related immunodeficiency?
["immunoglobulin deficiency", "intestinal inflammation"]