[5][6] SP-A1 is primarily synthesised in type II alveolar cells in the lung, as part of a complex of lipids and proteins known as pulmonary surfactant.

The protein component of surfactant helps in the modulation of the innate immune response, and inflammatory processes.

[10][11][12][13] The lung is the main site of SFTPA1 synthesis, but SFTPA1 mRNA expression has also been detected in the trachea, prostate, pancreas, thymus, colon, eye, salivary gland and other tissues.

[15][16] The expression of SFTPA1 is regulated by cellular factors including proteins, small RNAs (microRNAs), glucocorticoids, etc.

[17] Differences in the SFTPA1 gene sequence at the coding region determine SP-A genetic variants or haplotypes among individuals.

The amino acid differences that distinguish among SFTPA1 variants are located both at the carbohydrate recognition and the collagen-like domains.

Some of the functions by which both SFTPA1 and SFTPA2 contribute to innate immunity include: Environmental insults such as air pollution, and exposure to high concentrations of ozone and particulate matter can affect SP-A expression and function, via mechanisms that involve epigenetic regulation of SFTPA1 expression.

The ratio of SP-A1 to total SP-A has been correlated with lung disease (e.g. asthma, cystic fibrosis) and aging.

[30] The AD' form is the most represented among SFTPA1 transcripts (81%),[29] and experimental work has shown that this sequence can stabilize mRNA and enhance translation, but the mechanisms implicated in this regulation are still under investigation.

[32] The impact of this regulation on SFTPA1 and SFTPA2 protein levels may contribute to individual differences in susceptibility to lung disease.